The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Ding Yuan - One of the best experts on this subject based on the ideXlab platform.
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saponins from Panax japonicus alleviate hfd induced impaired behaviors through inhibiting nlrp3 inflammasome to upregulate ampa receptors
Neurochemistry International, 2021Co-Authors: Jinxin Wang, Changcheng Zhang, Ding Yuan, Zhiyong Zhou, Chaoqi Liu, Xulan Zhang, Chengfu Yuan, Dongfan Wang, Ting WangAbstract:Obesity is characterized by a condition of low-grade chronic inflammation that facilitates development of numerous comorbidities and dysregulation of brain homeostasis. It is reported that obesity can lead to behavioral alterations such as cognitive decline and depression-like behaviors both in humans and rodents. Saponins from Panax japonicus (SPJ) have been reported to exhibit anti-inflammatory action in mouse model of diet-induced obesity. We evaluated the neuroprotection of SPJ on high fat diet (HFD) induced impaired behaviors such as memory deficit and depressive-like behaviors, and explored the underlying mechanisms. 6-week male Balb/c mice were divided into normal control group (NC, 17% total calories from fat), HFD group (60% total calories from fat), and HFD treated with SPJ groups (orally gavaged with dosages of 15 mg/kg and 45 mg/kg), respectively. After treatment for 16 weeks, behavioral tests were performed to evaluate the cognition and depression-like behaviors of the mice. The underling mechanisms of SPJ on HFD-induced impaired behaviors were investigated through histopathological observation, western blot analysis and immunofluorescence. Our results showed that HFD-fed mice caused behavioral disorders, neuronal degeneration as well as elevated neuroinflammation, which was partly involved in NLRP3 inflammasome that finally resulted in decreased protein levels of AMPA receptors and down-regulated phosphorylated levels of CaMKII and CREB in cortex and hippocampus. All the above changes in cortex and hippocampus induced by HFD were mitigated by SPJ treatment. SPJ treatment alleviated HFD-induced recognitive impairment and depression-like behaviors of mice, which could be partly due to the capacity of SPJ to mitigate neuroinflammation through inhibition of NLRP3 inflammasome and upregulation of AMPA receptors signaling pathway.
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effect of total saponins from Panax japonicus on non alcoholic steatohepatitis by regulating autophagy
China journal of Chinese materia medica, 2021Co-Authors: Yue Luo, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Ting Wang, Chengfu YuanAbstract:Non-alcoholic steatohepatitis(NASH) was induced by high-sugar and high-fat diet in mice to investigate the intervention effect of total saponins from Panax japonicus(TSPJ) and explore its possible mechanism. Mice were fed with high-sugar and high-fat diet to establish NASH model, and intervened with different doses of TSPJ(15, 45 mg·kg~(-1)). The animals were fed for 26 weeks. The histomorphology and pathological changes of liver tissues were observed by HE staining. The transcriptional expression levels of miR-199 a-5 p, autophagy related gene 5(ATG5) and inflammatory cytokines interleukin-6(IL-6), interleukin-1β(IL-1β) and tumor necrosis factor α(TNF-α) in mouse liver were measured by quantitative Real-time polymerase chain reaction(qRT-PCR). Western blot was used to detect the expression of autophagy-related proteins ATG5, P62/SQSTM1(P62), and microtubule-associated protein light chain 3(LC3)-I/Ⅱ proteins in mouse liver. The expression of P62 protein was detected by immunofluorescence staining. In order to verify the targeting regulation relationship between miR-199 a-5 p and ATG5, miR mimic/inhibitor NC and miR-199 a-5 p mimic/inhibitor were transfected into Hepa 1-6 cells, and the expression of ATG5 mRNA and protein was detected. pMIR-reportor ATG5-3'UTR luciferase reporter gene plasmid was constructed and co-transfected with miR mimic/inhibitor NC and miR-199 a-5 p mimic/inhibitor into Hepa 1-6 cells to detect luciferase activity. In vivo, HE staining in the model group showed typical fatty degeneration and inflammatory infiltration, with increased expression of miR-199 a-5 p and decreased expression of ATG5 mRNA and protein. The expression of autophagy-associated protein P62 increased significantly, the ratio of LC3Ⅱ/Ⅰ decreased, and the transcriptional expression of inflammatory factors increased significantly. After the intervention by TSPJ, the pathological performance of liver tissue was significantly improved, the expression of miR-199 a-5 p decreased and the expression of ATG5 mRNA and protein increased, the expression of autophagy-associated protein P62 decreased significantly, the ratio of LC3Ⅱ/Ⅰ increased, and the transcriptional expression of inflammatory cytokines IL-6, IL-1β and TNF-α decreased significantly. In vitro, it was found that the expression of ATG5 mRNA and protein and luciferase activity decreased significantly in miR-199 a-5 p overexpression cells, while after inhibition of miR-199 a-5 p expression, the expression level of ATG5 mRNA and protein and luciferase activity increased. The results showed that TSPJ can improve NASH in mice fed with high-sugar and high-fat diet, and its mechanism may be related to the regulation of miR-199 a-5 p/ATG5 signal pathway, the regulation of autophagy activity and the improvement of inflammatory response of NASH.
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saponins from Panax japonicus ameliorate age related renal fibrosis by inhibition of inflammation mediated by nf κb and tgf β1 smad signaling and suppression of oxidative stress via activation of nrf2 are signaling
Journal of Ginseng Research, 2021Co-Authors: Yan Gao, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Yue Shi, Liyue Gai, Gang Zhou, Chengfu YuanAbstract:Background The decreased renal function is known to be associated with biological aging, of which the main pathological features are chronic inflammation and renal interstitial fibrosis. In previous studies, we reported that total saponins from Panax japonicus (SPJs) can availably protect acute myocardial ischemia. We proposed that SPJs might have similar protective effects for aging-associated renal interstitial fibrosis. Thus, in the present study, we evaluated the overall effect of SPJs on renal fibrosis. Methods Sprague-Dawley (SD) aging rats were given SPJs by gavage beginning from 18 months old, at 10 mg/kg/d and 60 mg/kg/d, up to 24 months old. After the experiment, changes in morphology, function and fibrosis of their kidneys were detected. The levels of serum uric acid (UA), β2-microglobulin (β2-MG) and cystatin C (Cys C) were assayed with ELISA kits. The levels of extracellular matrix (ECM), matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), inflammatory factors and changes of oxidative stress parameters were examined. Results After SPJs treatment, SD rats showed significantly histopathological changes in kidneys accompanied by decreased renal fibrosis and increased renal function; As compared with those in 3-month group, the levels of serum UA, Cys C and β2-MG in 24-month group were significantly increased (p < 0.05). Compared with those in the 24-month group, the levels of serum UA, Cys C and β2-MG in the SPJ-H group were significantly decreased. While ECM was reduced and the levels of MMP-2 and MMP-9 were increased, the levels of TIMP-1, TIMP-2 and transforming growth factor-β1 (TGF-β1)/Smad signaling were decreased; the expression level of phosphorylated nuclear factor kappa-B (NF-κB) was down-regulated with reduced inflammatory factors; meanwhile, the expression of nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) signaling was aggrandized. Conclusion These results suggest that SPJs treatment can improve age-associated renal fibrosis by inhibiting TGF-β1/Smad, NFκB signaling pathways and activating Nrf2-ARE signaling pathways and that SPJs can be a potentially valuable anti-renal fibrosis drug.
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the preventive effect of total saponins from Panax japonicus on inflammation and insulin resistance in adipose tissue of mice induced by a high fat diet
Journal of Functional Foods, 2021Co-Authors: Yue Shi, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Zhengtai Liu, Liyue Gai, Yan Gao, Gang Zhou, Chengfu YuanAbstract:Abstract We aimed to investigate the effects of total saponins from Panax japonicus (TSPJ) on adipocyte inflammation and insulin resistance induced by a high-fat diet (HFD). Moreover, its underlying mechanism was further explored. In vivo, we found that TSPJ inhibited the activation of NF-κB and increase the transcription of p-AKT, leading to reduced inflammation and improved sensitivity of adipocytes to insulin. In vitro evaluation revealed that palmitic acid (PA) induced inflammation by activating the NF-κB pathway, and triggered insulin resistance by affecting the expression of p-AKT in adipocytes. Treatment with 30 mg/kg and 90 mg/kg TSJP in animals and pre-treatment with 25 μg/mL and 50 μg/mL TSJP in 3T3-L1 could inhibit inflammation and insulin resistance induced by HFD and PA. Our study showed that TSPJ inhibited adipocyte inflammation by inhibiting the NF-κB pathway. Besides, TSPJ could also affect the expression of p-AKT to increase insulin sensitivity in adipocytes via targeting AMPK.
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protective effects of saponins from Panax japonicus on neurons of the colon myenteric plexus in aging rats through reduction of α synuclein through endoplasmic reticulum stress
Geriatrics & Gerontology International, 2021Co-Authors: Yuhui Guo, Jie Liu, Ding Yuan, Yaoyan Dun, Zhihao Cheng, Zhengguo Xiong, Changcheng ZhangAbstract:Aim The enteric nervous system degenerates gradually with age, and α-synuclein (α-syn) is a suitable marker of enteric nervous system degeneration, which is intimately related with endoplasmic reticulum stress and unfolded protein response (UPRER ). Saponins from Panax japonicus (SPJ) have obvious protective effects on neurons in several degenerative disease models. Here, the study was designed to investigate whether SPJ could reverse the neuron degeneration through regulating the UPRER in the colon myenteric plexus of aging rats. Methods Aging rats had been treated with SPJ for 6 months since they were aged 18 months. Then, the colon samples were collected and neuron morphology in the myenteric plexus was observed. Immunohistochemistry staining was used to detect the expressions of NeuN, α-syn, GRP78 and three different UPRER branches. Double immunofluorescence was used to determine the co-localization of α-syn and NeuN, GRP78 and NeuN. Results Neurons degenerated in the colon myenteric plexus of aging rats, but co-localization of α-syn and NeuN increased. In addition, both the expressions of GRP78 and three UPRER branch signaling pathway proteins decreased in the colon myenteric plexus of aging rats. Treatment of SPJ almost alleviated the above effects in aging rats, except for ATF6. Conclusions SPJ could reverse the neuron loss caused by accumulation of α-syn in the myenteric plexus of colon in aging rats, which is potentially associated with increased GRP78 and most URPER changes. Geriatr Gerontol Int 2021; 21: 85-93.
Changcheng Zhang - One of the best experts on this subject based on the ideXlab platform.
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saponins from Panax japonicus alleviate hfd induced impaired behaviors through inhibiting nlrp3 inflammasome to upregulate ampa receptors
Neurochemistry International, 2021Co-Authors: Jinxin Wang, Changcheng Zhang, Ding Yuan, Zhiyong Zhou, Chaoqi Liu, Xulan Zhang, Chengfu Yuan, Dongfan Wang, Ting WangAbstract:Obesity is characterized by a condition of low-grade chronic inflammation that facilitates development of numerous comorbidities and dysregulation of brain homeostasis. It is reported that obesity can lead to behavioral alterations such as cognitive decline and depression-like behaviors both in humans and rodents. Saponins from Panax japonicus (SPJ) have been reported to exhibit anti-inflammatory action in mouse model of diet-induced obesity. We evaluated the neuroprotection of SPJ on high fat diet (HFD) induced impaired behaviors such as memory deficit and depressive-like behaviors, and explored the underlying mechanisms. 6-week male Balb/c mice were divided into normal control group (NC, 17% total calories from fat), HFD group (60% total calories from fat), and HFD treated with SPJ groups (orally gavaged with dosages of 15 mg/kg and 45 mg/kg), respectively. After treatment for 16 weeks, behavioral tests were performed to evaluate the cognition and depression-like behaviors of the mice. The underling mechanisms of SPJ on HFD-induced impaired behaviors were investigated through histopathological observation, western blot analysis and immunofluorescence. Our results showed that HFD-fed mice caused behavioral disorders, neuronal degeneration as well as elevated neuroinflammation, which was partly involved in NLRP3 inflammasome that finally resulted in decreased protein levels of AMPA receptors and down-regulated phosphorylated levels of CaMKII and CREB in cortex and hippocampus. All the above changes in cortex and hippocampus induced by HFD were mitigated by SPJ treatment. SPJ treatment alleviated HFD-induced recognitive impairment and depression-like behaviors of mice, which could be partly due to the capacity of SPJ to mitigate neuroinflammation through inhibition of NLRP3 inflammasome and upregulation of AMPA receptors signaling pathway.
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effect of total saponins from Panax japonicus on non alcoholic steatohepatitis by regulating autophagy
China journal of Chinese materia medica, 2021Co-Authors: Yue Luo, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Ting Wang, Chengfu YuanAbstract:Non-alcoholic steatohepatitis(NASH) was induced by high-sugar and high-fat diet in mice to investigate the intervention effect of total saponins from Panax japonicus(TSPJ) and explore its possible mechanism. Mice were fed with high-sugar and high-fat diet to establish NASH model, and intervened with different doses of TSPJ(15, 45 mg·kg~(-1)). The animals were fed for 26 weeks. The histomorphology and pathological changes of liver tissues were observed by HE staining. The transcriptional expression levels of miR-199 a-5 p, autophagy related gene 5(ATG5) and inflammatory cytokines interleukin-6(IL-6), interleukin-1β(IL-1β) and tumor necrosis factor α(TNF-α) in mouse liver were measured by quantitative Real-time polymerase chain reaction(qRT-PCR). Western blot was used to detect the expression of autophagy-related proteins ATG5, P62/SQSTM1(P62), and microtubule-associated protein light chain 3(LC3)-I/Ⅱ proteins in mouse liver. The expression of P62 protein was detected by immunofluorescence staining. In order to verify the targeting regulation relationship between miR-199 a-5 p and ATG5, miR mimic/inhibitor NC and miR-199 a-5 p mimic/inhibitor were transfected into Hepa 1-6 cells, and the expression of ATG5 mRNA and protein was detected. pMIR-reportor ATG5-3'UTR luciferase reporter gene plasmid was constructed and co-transfected with miR mimic/inhibitor NC and miR-199 a-5 p mimic/inhibitor into Hepa 1-6 cells to detect luciferase activity. In vivo, HE staining in the model group showed typical fatty degeneration and inflammatory infiltration, with increased expression of miR-199 a-5 p and decreased expression of ATG5 mRNA and protein. The expression of autophagy-associated protein P62 increased significantly, the ratio of LC3Ⅱ/Ⅰ decreased, and the transcriptional expression of inflammatory factors increased significantly. After the intervention by TSPJ, the pathological performance of liver tissue was significantly improved, the expression of miR-199 a-5 p decreased and the expression of ATG5 mRNA and protein increased, the expression of autophagy-associated protein P62 decreased significantly, the ratio of LC3Ⅱ/Ⅰ increased, and the transcriptional expression of inflammatory cytokines IL-6, IL-1β and TNF-α decreased significantly. In vitro, it was found that the expression of ATG5 mRNA and protein and luciferase activity decreased significantly in miR-199 a-5 p overexpression cells, while after inhibition of miR-199 a-5 p expression, the expression level of ATG5 mRNA and protein and luciferase activity increased. The results showed that TSPJ can improve NASH in mice fed with high-sugar and high-fat diet, and its mechanism may be related to the regulation of miR-199 a-5 p/ATG5 signal pathway, the regulation of autophagy activity and the improvement of inflammatory response of NASH.
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saponins from Panax japonicus ameliorate age related renal fibrosis by inhibition of inflammation mediated by nf κb and tgf β1 smad signaling and suppression of oxidative stress via activation of nrf2 are signaling
Journal of Ginseng Research, 2021Co-Authors: Yan Gao, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Yue Shi, Liyue Gai, Gang Zhou, Chengfu YuanAbstract:Background The decreased renal function is known to be associated with biological aging, of which the main pathological features are chronic inflammation and renal interstitial fibrosis. In previous studies, we reported that total saponins from Panax japonicus (SPJs) can availably protect acute myocardial ischemia. We proposed that SPJs might have similar protective effects for aging-associated renal interstitial fibrosis. Thus, in the present study, we evaluated the overall effect of SPJs on renal fibrosis. Methods Sprague-Dawley (SD) aging rats were given SPJs by gavage beginning from 18 months old, at 10 mg/kg/d and 60 mg/kg/d, up to 24 months old. After the experiment, changes in morphology, function and fibrosis of their kidneys were detected. The levels of serum uric acid (UA), β2-microglobulin (β2-MG) and cystatin C (Cys C) were assayed with ELISA kits. The levels of extracellular matrix (ECM), matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), inflammatory factors and changes of oxidative stress parameters were examined. Results After SPJs treatment, SD rats showed significantly histopathological changes in kidneys accompanied by decreased renal fibrosis and increased renal function; As compared with those in 3-month group, the levels of serum UA, Cys C and β2-MG in 24-month group were significantly increased (p < 0.05). Compared with those in the 24-month group, the levels of serum UA, Cys C and β2-MG in the SPJ-H group were significantly decreased. While ECM was reduced and the levels of MMP-2 and MMP-9 were increased, the levels of TIMP-1, TIMP-2 and transforming growth factor-β1 (TGF-β1)/Smad signaling were decreased; the expression level of phosphorylated nuclear factor kappa-B (NF-κB) was down-regulated with reduced inflammatory factors; meanwhile, the expression of nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) signaling was aggrandized. Conclusion These results suggest that SPJs treatment can improve age-associated renal fibrosis by inhibiting TGF-β1/Smad, NFκB signaling pathways and activating Nrf2-ARE signaling pathways and that SPJs can be a potentially valuable anti-renal fibrosis drug.
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the preventive effect of total saponins from Panax japonicus on inflammation and insulin resistance in adipose tissue of mice induced by a high fat diet
Journal of Functional Foods, 2021Co-Authors: Yue Shi, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Zhengtai Liu, Liyue Gai, Yan Gao, Gang Zhou, Chengfu YuanAbstract:Abstract We aimed to investigate the effects of total saponins from Panax japonicus (TSPJ) on adipocyte inflammation and insulin resistance induced by a high-fat diet (HFD). Moreover, its underlying mechanism was further explored. In vivo, we found that TSPJ inhibited the activation of NF-κB and increase the transcription of p-AKT, leading to reduced inflammation and improved sensitivity of adipocytes to insulin. In vitro evaluation revealed that palmitic acid (PA) induced inflammation by activating the NF-κB pathway, and triggered insulin resistance by affecting the expression of p-AKT in adipocytes. Treatment with 30 mg/kg and 90 mg/kg TSJP in animals and pre-treatment with 25 μg/mL and 50 μg/mL TSJP in 3T3-L1 could inhibit inflammation and insulin resistance induced by HFD and PA. Our study showed that TSPJ inhibited adipocyte inflammation by inhibiting the NF-κB pathway. Besides, TSPJ could also affect the expression of p-AKT to increase insulin sensitivity in adipocytes via targeting AMPK.
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protective effects of saponins from Panax japonicus on neurons of the colon myenteric plexus in aging rats through reduction of α synuclein through endoplasmic reticulum stress
Geriatrics & Gerontology International, 2021Co-Authors: Yuhui Guo, Jie Liu, Ding Yuan, Yaoyan Dun, Zhihao Cheng, Zhengguo Xiong, Changcheng ZhangAbstract:Aim The enteric nervous system degenerates gradually with age, and α-synuclein (α-syn) is a suitable marker of enteric nervous system degeneration, which is intimately related with endoplasmic reticulum stress and unfolded protein response (UPRER ). Saponins from Panax japonicus (SPJ) have obvious protective effects on neurons in several degenerative disease models. Here, the study was designed to investigate whether SPJ could reverse the neuron degeneration through regulating the UPRER in the colon myenteric plexus of aging rats. Methods Aging rats had been treated with SPJ for 6 months since they were aged 18 months. Then, the colon samples were collected and neuron morphology in the myenteric plexus was observed. Immunohistochemistry staining was used to detect the expressions of NeuN, α-syn, GRP78 and three different UPRER branches. Double immunofluorescence was used to determine the co-localization of α-syn and NeuN, GRP78 and NeuN. Results Neurons degenerated in the colon myenteric plexus of aging rats, but co-localization of α-syn and NeuN increased. In addition, both the expressions of GRP78 and three UPRER branch signaling pathway proteins decreased in the colon myenteric plexus of aging rats. Treatment of SPJ almost alleviated the above effects in aging rats, except for ATF6. Conclusions SPJ could reverse the neuron loss caused by accumulation of α-syn in the myenteric plexus of colon in aging rats, which is potentially associated with increased GRP78 and most URPER changes. Geriatr Gerontol Int 2021; 21: 85-93.
Ting Wang - One of the best experts on this subject based on the ideXlab platform.
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saponins from Panax japonicus alleviate hfd induced impaired behaviors through inhibiting nlrp3 inflammasome to upregulate ampa receptors
Neurochemistry International, 2021Co-Authors: Jinxin Wang, Changcheng Zhang, Ding Yuan, Zhiyong Zhou, Chaoqi Liu, Xulan Zhang, Chengfu Yuan, Dongfan Wang, Ting WangAbstract:Obesity is characterized by a condition of low-grade chronic inflammation that facilitates development of numerous comorbidities and dysregulation of brain homeostasis. It is reported that obesity can lead to behavioral alterations such as cognitive decline and depression-like behaviors both in humans and rodents. Saponins from Panax japonicus (SPJ) have been reported to exhibit anti-inflammatory action in mouse model of diet-induced obesity. We evaluated the neuroprotection of SPJ on high fat diet (HFD) induced impaired behaviors such as memory deficit and depressive-like behaviors, and explored the underlying mechanisms. 6-week male Balb/c mice were divided into normal control group (NC, 17% total calories from fat), HFD group (60% total calories from fat), and HFD treated with SPJ groups (orally gavaged with dosages of 15 mg/kg and 45 mg/kg), respectively. After treatment for 16 weeks, behavioral tests were performed to evaluate the cognition and depression-like behaviors of the mice. The underling mechanisms of SPJ on HFD-induced impaired behaviors were investigated through histopathological observation, western blot analysis and immunofluorescence. Our results showed that HFD-fed mice caused behavioral disorders, neuronal degeneration as well as elevated neuroinflammation, which was partly involved in NLRP3 inflammasome that finally resulted in decreased protein levels of AMPA receptors and down-regulated phosphorylated levels of CaMKII and CREB in cortex and hippocampus. All the above changes in cortex and hippocampus induced by HFD were mitigated by SPJ treatment. SPJ treatment alleviated HFD-induced recognitive impairment and depression-like behaviors of mice, which could be partly due to the capacity of SPJ to mitigate neuroinflammation through inhibition of NLRP3 inflammasome and upregulation of AMPA receptors signaling pathway.
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effect of total saponins from Panax japonicus on non alcoholic steatohepatitis by regulating autophagy
China journal of Chinese materia medica, 2021Co-Authors: Yue Luo, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Ting Wang, Chengfu YuanAbstract:Non-alcoholic steatohepatitis(NASH) was induced by high-sugar and high-fat diet in mice to investigate the intervention effect of total saponins from Panax japonicus(TSPJ) and explore its possible mechanism. Mice were fed with high-sugar and high-fat diet to establish NASH model, and intervened with different doses of TSPJ(15, 45 mg·kg~(-1)). The animals were fed for 26 weeks. The histomorphology and pathological changes of liver tissues were observed by HE staining. The transcriptional expression levels of miR-199 a-5 p, autophagy related gene 5(ATG5) and inflammatory cytokines interleukin-6(IL-6), interleukin-1β(IL-1β) and tumor necrosis factor α(TNF-α) in mouse liver were measured by quantitative Real-time polymerase chain reaction(qRT-PCR). Western blot was used to detect the expression of autophagy-related proteins ATG5, P62/SQSTM1(P62), and microtubule-associated protein light chain 3(LC3)-I/Ⅱ proteins in mouse liver. The expression of P62 protein was detected by immunofluorescence staining. In order to verify the targeting regulation relationship between miR-199 a-5 p and ATG5, miR mimic/inhibitor NC and miR-199 a-5 p mimic/inhibitor were transfected into Hepa 1-6 cells, and the expression of ATG5 mRNA and protein was detected. pMIR-reportor ATG5-3'UTR luciferase reporter gene plasmid was constructed and co-transfected with miR mimic/inhibitor NC and miR-199 a-5 p mimic/inhibitor into Hepa 1-6 cells to detect luciferase activity. In vivo, HE staining in the model group showed typical fatty degeneration and inflammatory infiltration, with increased expression of miR-199 a-5 p and decreased expression of ATG5 mRNA and protein. The expression of autophagy-associated protein P62 increased significantly, the ratio of LC3Ⅱ/Ⅰ decreased, and the transcriptional expression of inflammatory factors increased significantly. After the intervention by TSPJ, the pathological performance of liver tissue was significantly improved, the expression of miR-199 a-5 p decreased and the expression of ATG5 mRNA and protein increased, the expression of autophagy-associated protein P62 decreased significantly, the ratio of LC3Ⅱ/Ⅰ increased, and the transcriptional expression of inflammatory cytokines IL-6, IL-1β and TNF-α decreased significantly. In vitro, it was found that the expression of ATG5 mRNA and protein and luciferase activity decreased significantly in miR-199 a-5 p overexpression cells, while after inhibition of miR-199 a-5 p expression, the expression level of ATG5 mRNA and protein and luciferase activity increased. The results showed that TSPJ can improve NASH in mice fed with high-sugar and high-fat diet, and its mechanism may be related to the regulation of miR-199 a-5 p/ATG5 signal pathway, the regulation of autophagy activity and the improvement of inflammatory response of NASH.
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saponins from Panax japonicus attenuate cognitive impairment in ageing rats through regulating microglial polarisation and autophagy
Pharmaceutical Biology, 2021Co-Authors: Qingqing Zhao, Changcheng Zhang, Ding Yuan, Zhiyong Zhou, Jinxin Wang, Xulan Zhang, Ting WangAbstract:Context Panax japonicus is the dried rhizome of Panax japonicus C.A. Mey. (Araliaceae). Saponins from Panax japonicus (SPJ) exhibit anti-inflammatory and antioxidative effects. Objective To explore the neuroprotective effect of SPJ on natural ageing of rat. Materials and methods Sprague-Dawley (SD) rats 18-month-old were divided into ageing control, ageing treated with SPJ 10 or 30 mg/kg (n = 8). Five-month-old rats were taken as the adult control (n = 8). Rats were fed regular feed or feed containing SPJ for 4 months. Cognitive level was evaluated by Morris water maze (MWM) test. The mechanisms of SPJ's neuroprotection were evaluated by transmission electron microscope, western blot analysis, and immunofluorescence in vivo and in vitro. Results SPJ attenuated ageing-induced cognitive impairment as indicated by elevated number of times crossing the target platform (from 1.63 to 3.5) and longer time spent in the target platform quadrant (from 1.33 to 1.98). Meanwhile, SPJ improved the morphology of microglia and synapse, and activated M2 microglia polarisation including increased hippocampus levels of CD206 (from 0.98 to 1.47) and YM-1 (from 0.67 to 1.1), and enhanced autophagy-related proteins LC3B (from 0.48 to 0.82), Beclin1 (from 0.32 to 0.51), Atg5 (from 0.22 to 0.89) whereas decreased p62 level (from 0.71 to 0.45) of ageing rats. In vitro study also showed that SPJ regulated the microglial polarisation and autophagy. Discussion and conclusions SPJ improved cognitive deficits of ageing rats through attenuating microglial inflammation and enhancing microglial autophagy, which could be used to treat neurodegenerative disorders.
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improved effects of saponins from Panax japonicus on decline of cognitive function in natural aging rats via nlrp3 inflammasome pathway
China journal of Chinese materia medica, 2019Co-Authors: Bo Ruan, Changcheng Zhang, Ding Yuan, Zhiyong Zhou, Yuanjian Yang, Rui Wang, Dongfan Wang, Jiawen Wang, Ting WangAbstract:The aim of this paper was to investigate the effect of total saponins from Panax japonicus( SPJ) on cognitive decline of natural aging rats and its mechanism. Thirty male SD rats of eighteen month old were randomly divided into three groups: aged group,10 mg·kg~(-1) SPJ-treated group and 30 mg·kg~(-1) SPJ-treated group. The SPJ-treated groups were given SPJ at the dosages of 10 mg·kg~(-1) and 30 mg·kg~(-1),respectively,from the age of 18 to 24 months. Aged group were lavaged the same amount of saline,10 six-month-old rats were used as control group,with 10 rats in each group. The open field test,novel object recognition and Morris water maze were performed to detect the changes of cognitive function in each group. The changes of synaptic transmission of long-term potentiation( LTP) in hippocampal CA1 region were detected by field potential recording. Western blot was used to detect the protein levels of NLRP3,ASC,caspase-1 and the changes of Glu A1,Glu A2,CAMKⅡ,CREB and phosphorylation of CAMKⅡ,CREB in each group.The results showed that SPJ could improve the decline of cognitive function in aging rats,reduce the damage of LTP in the hippocampal CA1 region of aged rats,and decrease the expression of NLRP3,ASC,caspase-1 in aging rats. At the same time,SPJ could enhance the membrane expression of AMPA receptor( Glu A1 and Glu A2),and increase the expression of p-CAMKⅡand p-CREB in aging rats.SPJ could improve cognitive decline of natural aging rats,and its mechanism may be related to regulating NLRP3 inflammasome,thus regulating the membrane expression of AMPA receptor,and enhancing the expression phosphorylation of CAMKⅡ and CREB.
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regulatory effects of saponins from Panax japonicus on colonic epithelial tight junctions in aging rats
Journal of Ginseng Research, 2018Co-Authors: Yaoyan Dun, Haixia Zhao, Zhiyong Zhou, Chaoqi Liu, Ting Wang, Min Liu, Jing Chen, Danli Peng, Yuhui Guo, Changcheng ZhangAbstract:Abstract Background Saponins from Panax japonicus (SPJ) are the most abundant and main active components of P. japonicus , which replaces ginseng roots in treatment for many kinds of diseases in the minority ethnic group in China. Our previous studies have demonstrated that SPJ has the effects of anti-inflammation through the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways. The present study was designed to investigate whether SPJ can modulate intestinal tight junction barrier in aging rats and further to explore the potential mechanism. Methods Aging rats had been treated with different doses (10 mg/kg, 30 mg/kg, and 60 mg/kg) of SPJ for 6 mo since they were 18 mo old. After the rats were euthanized, the colonic samples were harvested. Levels of tight junctions (claudin-1 and occludin) were determined by immunohistochemical staining. Levels of proinflammatory cytokines (interleukin-1β and tumor necrosis factor-α) were examined by Western blot. NF-κB and phosphorylation of MAPK signaling pathways were also determined by Western blot. Results We found that SPJ increased the expression of the tight junction proteins claudin-1 and occludin in the colon of aging rats. Treatment with SPJ decreased the levels of interleukin-1β and tumor necrosis factor-α, reduced the phosphorylation of three MAPK isoforms, and inhibited the expression of NF-κB in the colon of aging rats. Conclusion The studies demonstrated that SPJ modulates the damage of intestinal epithelial tight junction in aging rats, inhibits inflammation, and downregulates the phosphorylation of the MAPK and NF-κB signaling pathways.
Yaoyan Dun - One of the best experts on this subject based on the ideXlab platform.
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protective effects of saponins from Panax japonicus on neurons of the colon myenteric plexus in aging rats through reduction of α synuclein through endoplasmic reticulum stress
Geriatrics & Gerontology International, 2021Co-Authors: Yuhui Guo, Jie Liu, Ding Yuan, Yaoyan Dun, Zhihao Cheng, Zhengguo Xiong, Changcheng ZhangAbstract:Aim The enteric nervous system degenerates gradually with age, and α-synuclein (α-syn) is a suitable marker of enteric nervous system degeneration, which is intimately related with endoplasmic reticulum stress and unfolded protein response (UPRER ). Saponins from Panax japonicus (SPJ) have obvious protective effects on neurons in several degenerative disease models. Here, the study was designed to investigate whether SPJ could reverse the neuron degeneration through regulating the UPRER in the colon myenteric plexus of aging rats. Methods Aging rats had been treated with SPJ for 6 months since they were aged 18 months. Then, the colon samples were collected and neuron morphology in the myenteric plexus was observed. Immunohistochemistry staining was used to detect the expressions of NeuN, α-syn, GRP78 and three different UPRER branches. Double immunofluorescence was used to determine the co-localization of α-syn and NeuN, GRP78 and NeuN. Results Neurons degenerated in the colon myenteric plexus of aging rats, but co-localization of α-syn and NeuN increased. In addition, both the expressions of GRP78 and three UPRER branch signaling pathway proteins decreased in the colon myenteric plexus of aging rats. Treatment of SPJ almost alleviated the above effects in aging rats, except for ATF6. Conclusions SPJ could reverse the neuron loss caused by accumulation of α-syn in the myenteric plexus of colon in aging rats, which is potentially associated with increased GRP78 and most URPER changes. Geriatr Gerontol Int 2021; 21: 85-93.
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saponins of Panax japonicus confer neuroprotection against brain aging through mitochondrial related oxidative stress and autophagy in rats
Current Pharmaceutical Biotechnology, 2020Co-Authors: Jingzhi Wan, Changcheng Zhang, Haixia Zhao, Lili Deng, Zhiyong Zhou, Chaoqi Liu, Yaoyan Dun, Rui Wang, Chengfu Yuan, Ding YuanAbstract:Background Oxidative stress and mitochondrial dysfunction play a vital role in the pathogenesis of brain aging. Saponins from Panax japonicus (SPJ) have attracted much attention for their potential to attenuate age-related oxidative stress as the main ingredient in rhizomes of Panax japonicus. Objective This study aimed to investigate the neuroprotective effects of SPJ on natural aging rats as well as the underlying mechanisms regarding oxidative stress and mitochondrial pathway. Methods Sprague-Dawley rats were divided into control groups (3-, 9-, 15- and 24-month old groups) and SPJ-treated groups. For SPJ-treated groups, SPJ were orally administrated to 18-month old rats at doses of 10 mg/kg, 30 mg/kg and 60 mg/kg once daily. Control groups were given the same volume of saline. After the treatment with SPJ or saline for six months, the cortex and hippocampus were rapidly harvested and deposited at -80°C after the rats were decapitated under anesthesia. The neuroprotective effects of SPJ were estimated by histopathological observation, TUNEL detection, biochemical determination and western blotting. Results SPJ improved pathomorphological changes in neuronal cells and decreased apoptosis in the cortex and hippocampus of aging rats, increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), Na+/K+-ATPase, Ca2+-ATPase and Ca2+/Mg2+-ATPase whereas, decreased malondialdehyde (MDA) contents in the cortex of aging rats. Furthermore, the SPJ increased silent mating type information regulation 2 homolog-1 (SIRT1) protein expression, decreased acetylated level of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in the cortex and hippocampus of aging rats, and reversed the aging-induced decline of Forkhead box O3 (Foxo3a), Superoxide Dismutase 2 (SOD2), microtubule-associated protein light chain 3 (LC3II) and Beclin1 levels in the cortex and hippocampus. Conclusion Our data showed that SPJ conferred neuroprotection partly through the regulation of oxidative stress and mitochondria-related pathways in aging rats.
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distinct expression patterns of aging effects on the uprer signaling pathway in rat colon and regulatory role of saponins from Panax japonicus
International Journal of Clinical and Experimental Pathology, 2019Co-Authors: Yaoyan Dun, Jie Liu, Ding Yuan, Yuhui Guo, Zhihao Cheng, Zhengguo Xiong, Changcheng ZhangAbstract:Background Studies have reported that the unfolded protein response of ER (UPRER) declines in the several organs of aging mice. However, changes of UPRER during the aging process in the intestine are rarely reported. Our previous studies have demonstrated that Saponins from Panax japonicus (SPJ) have anti-aging effects in different murine models and can modulate ER stress. In the present study, we focused on age-dependent expressions of UPRER in the intestine of 6- to 24-month-old rats by an immunohistochemical (IHC) method and determined whether SPJ could regulate the three different UPRER branches of the colon in aging rats. Methods Aging rats had been treated with different doses (10 and 30 mg/kg) of SPJ for 6 months, which were mixed with feed, since they were 18 months old. Then the expressions of GRP78 and three different UPRER branches were determined by immunohistochemistry (IHC). Results: Total expressions of GRP78 and p-JNK increased, and other UPRER proteins decreased in the colon of aging rats, while SPJ treatment relieved the corresponding changes in aging rats. Here we also found different patterns of GRP78 and the three UPRER branches in the different layers of colon in rats. Conclusion The study demonstrated that UPRER declined and GRP78 increased in the colon of aging rats. SPJ could reverse most URPER changes in the colon of aging rats. This study also showed different expression patterns of the three branches of UPRER in different layers of the colon in rats.
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regulatory effects of saponins from Panax japonicus on colonic epithelial tight junctions in aging rats
Journal of Ginseng Research, 2018Co-Authors: Yaoyan Dun, Haixia Zhao, Zhiyong Zhou, Chaoqi Liu, Ting Wang, Min Liu, Jing Chen, Danli Peng, Yuhui Guo, Changcheng ZhangAbstract:Abstract Background Saponins from Panax japonicus (SPJ) are the most abundant and main active components of P. japonicus , which replaces ginseng roots in treatment for many kinds of diseases in the minority ethnic group in China. Our previous studies have demonstrated that SPJ has the effects of anti-inflammation through the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways. The present study was designed to investigate whether SPJ can modulate intestinal tight junction barrier in aging rats and further to explore the potential mechanism. Methods Aging rats had been treated with different doses (10 mg/kg, 30 mg/kg, and 60 mg/kg) of SPJ for 6 mo since they were 18 mo old. After the rats were euthanized, the colonic samples were harvested. Levels of tight junctions (claudin-1 and occludin) were determined by immunohistochemical staining. Levels of proinflammatory cytokines (interleukin-1β and tumor necrosis factor-α) were examined by Western blot. NF-κB and phosphorylation of MAPK signaling pathways were also determined by Western blot. Results We found that SPJ increased the expression of the tight junction proteins claudin-1 and occludin in the colon of aging rats. Treatment with SPJ decreased the levels of interleukin-1β and tumor necrosis factor-α, reduced the phosphorylation of three MAPK isoforms, and inhibited the expression of NF-κB in the colon of aging rats. Conclusion The studies demonstrated that SPJ modulates the damage of intestinal epithelial tight junction in aging rats, inhibits inflammation, and downregulates the phosphorylation of the MAPK and NF-κB signaling pathways.
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saponins from Panax japonicus attenuate age related neuroinflammation via regulation of the mitogen activated protein kinase and nuclear factor kappa b signaling pathways
Neural Regeneration Research, 2017Co-Authors: Lili Deng, Changcheng Zhang, Haixia Zhao, Ding Yuan, Zhiyong Zhou, Jingzhi Wan, Chaoqi Liu, Yaoyan Dun, Bo Zhao, Yuanjian YangAbstract:Neuroinflammation is recognized as an important pathogenic factor for aging and related cognitive disorders. Mitogen-activated protein kinase and nuclear factor kappa B signaling pathways may mediate neuroinflammation. Saponins from Panax japonicus are the most abundant and bioactive members in rhizomes of Panax japonicus, and show anti-inflammatory activity. However, it is not known whether saponin from Panax japonicus has an anti-inflammatory effect in the aging brain, and likewise its underlying mechanisms. Sprague-Dawley rats were divided into control groups (3-, 9-, 15-, and 24-month-old groups) and saponins from Panax japonicus-treated groups. Saponins from Panax japonicus-treated groups were orally administrated saponins from Panax japonicus at three doses of 10, 30, and 60 mg/kg once daily for 6 months until the rats were 24 months old. Immunohistochemical staining and western blot assay results demonstrated that many microglia were activated in 24-month-old rats compared with 3- and 9-month-old rats. Expression of interleukin-1β, tumor necrosis factor-α, cyclooxygenase-2, and inducible nitric oxide synthase increased. Each dose of saponins from Panax japonicus visibly suppressed microglial activation in the aging rat brain, and inhibited expression levels of the above factors. Each dose of saponins from Panax japonicus markedly diminished levels of nuclear factor kappa B, IκBα, extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38. These results confirm that saponins from Panax japonicus can mitigate neuroinflammation in the aging rat brain by inhibition of the mitogen-activated protein kinase and nuclear factor kappa B signaling pathways.
Chaoqi Liu - One of the best experts on this subject based on the ideXlab platform.
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saponins from Panax japonicus alleviate hfd induced impaired behaviors through inhibiting nlrp3 inflammasome to upregulate ampa receptors
Neurochemistry International, 2021Co-Authors: Jinxin Wang, Changcheng Zhang, Ding Yuan, Zhiyong Zhou, Chaoqi Liu, Xulan Zhang, Chengfu Yuan, Dongfan Wang, Ting WangAbstract:Obesity is characterized by a condition of low-grade chronic inflammation that facilitates development of numerous comorbidities and dysregulation of brain homeostasis. It is reported that obesity can lead to behavioral alterations such as cognitive decline and depression-like behaviors both in humans and rodents. Saponins from Panax japonicus (SPJ) have been reported to exhibit anti-inflammatory action in mouse model of diet-induced obesity. We evaluated the neuroprotection of SPJ on high fat diet (HFD) induced impaired behaviors such as memory deficit and depressive-like behaviors, and explored the underlying mechanisms. 6-week male Balb/c mice were divided into normal control group (NC, 17% total calories from fat), HFD group (60% total calories from fat), and HFD treated with SPJ groups (orally gavaged with dosages of 15 mg/kg and 45 mg/kg), respectively. After treatment for 16 weeks, behavioral tests were performed to evaluate the cognition and depression-like behaviors of the mice. The underling mechanisms of SPJ on HFD-induced impaired behaviors were investigated through histopathological observation, western blot analysis and immunofluorescence. Our results showed that HFD-fed mice caused behavioral disorders, neuronal degeneration as well as elevated neuroinflammation, which was partly involved in NLRP3 inflammasome that finally resulted in decreased protein levels of AMPA receptors and down-regulated phosphorylated levels of CaMKII and CREB in cortex and hippocampus. All the above changes in cortex and hippocampus induced by HFD were mitigated by SPJ treatment. SPJ treatment alleviated HFD-induced recognitive impairment and depression-like behaviors of mice, which could be partly due to the capacity of SPJ to mitigate neuroinflammation through inhibition of NLRP3 inflammasome and upregulation of AMPA receptors signaling pathway.
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effect of total saponins from Panax japonicus on non alcoholic steatohepatitis by regulating autophagy
China journal of Chinese materia medica, 2021Co-Authors: Yue Luo, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Ting Wang, Chengfu YuanAbstract:Non-alcoholic steatohepatitis(NASH) was induced by high-sugar and high-fat diet in mice to investigate the intervention effect of total saponins from Panax japonicus(TSPJ) and explore its possible mechanism. Mice were fed with high-sugar and high-fat diet to establish NASH model, and intervened with different doses of TSPJ(15, 45 mg·kg~(-1)). The animals were fed for 26 weeks. The histomorphology and pathological changes of liver tissues were observed by HE staining. The transcriptional expression levels of miR-199 a-5 p, autophagy related gene 5(ATG5) and inflammatory cytokines interleukin-6(IL-6), interleukin-1β(IL-1β) and tumor necrosis factor α(TNF-α) in mouse liver were measured by quantitative Real-time polymerase chain reaction(qRT-PCR). Western blot was used to detect the expression of autophagy-related proteins ATG5, P62/SQSTM1(P62), and microtubule-associated protein light chain 3(LC3)-I/Ⅱ proteins in mouse liver. The expression of P62 protein was detected by immunofluorescence staining. In order to verify the targeting regulation relationship between miR-199 a-5 p and ATG5, miR mimic/inhibitor NC and miR-199 a-5 p mimic/inhibitor were transfected into Hepa 1-6 cells, and the expression of ATG5 mRNA and protein was detected. pMIR-reportor ATG5-3'UTR luciferase reporter gene plasmid was constructed and co-transfected with miR mimic/inhibitor NC and miR-199 a-5 p mimic/inhibitor into Hepa 1-6 cells to detect luciferase activity. In vivo, HE staining in the model group showed typical fatty degeneration and inflammatory infiltration, with increased expression of miR-199 a-5 p and decreased expression of ATG5 mRNA and protein. The expression of autophagy-associated protein P62 increased significantly, the ratio of LC3Ⅱ/Ⅰ decreased, and the transcriptional expression of inflammatory factors increased significantly. After the intervention by TSPJ, the pathological performance of liver tissue was significantly improved, the expression of miR-199 a-5 p decreased and the expression of ATG5 mRNA and protein increased, the expression of autophagy-associated protein P62 decreased significantly, the ratio of LC3Ⅱ/Ⅰ increased, and the transcriptional expression of inflammatory cytokines IL-6, IL-1β and TNF-α decreased significantly. In vitro, it was found that the expression of ATG5 mRNA and protein and luciferase activity decreased significantly in miR-199 a-5 p overexpression cells, while after inhibition of miR-199 a-5 p expression, the expression level of ATG5 mRNA and protein and luciferase activity increased. The results showed that TSPJ can improve NASH in mice fed with high-sugar and high-fat diet, and its mechanism may be related to the regulation of miR-199 a-5 p/ATG5 signal pathway, the regulation of autophagy activity and the improvement of inflammatory response of NASH.
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saponins from Panax japonicus ameliorate age related renal fibrosis by inhibition of inflammation mediated by nf κb and tgf β1 smad signaling and suppression of oxidative stress via activation of nrf2 are signaling
Journal of Ginseng Research, 2021Co-Authors: Yan Gao, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Yue Shi, Liyue Gai, Gang Zhou, Chengfu YuanAbstract:Background The decreased renal function is known to be associated with biological aging, of which the main pathological features are chronic inflammation and renal interstitial fibrosis. In previous studies, we reported that total saponins from Panax japonicus (SPJs) can availably protect acute myocardial ischemia. We proposed that SPJs might have similar protective effects for aging-associated renal interstitial fibrosis. Thus, in the present study, we evaluated the overall effect of SPJs on renal fibrosis. Methods Sprague-Dawley (SD) aging rats were given SPJs by gavage beginning from 18 months old, at 10 mg/kg/d and 60 mg/kg/d, up to 24 months old. After the experiment, changes in morphology, function and fibrosis of their kidneys were detected. The levels of serum uric acid (UA), β2-microglobulin (β2-MG) and cystatin C (Cys C) were assayed with ELISA kits. The levels of extracellular matrix (ECM), matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), inflammatory factors and changes of oxidative stress parameters were examined. Results After SPJs treatment, SD rats showed significantly histopathological changes in kidneys accompanied by decreased renal fibrosis and increased renal function; As compared with those in 3-month group, the levels of serum UA, Cys C and β2-MG in 24-month group were significantly increased (p < 0.05). Compared with those in the 24-month group, the levels of serum UA, Cys C and β2-MG in the SPJ-H group were significantly decreased. While ECM was reduced and the levels of MMP-2 and MMP-9 were increased, the levels of TIMP-1, TIMP-2 and transforming growth factor-β1 (TGF-β1)/Smad signaling were decreased; the expression level of phosphorylated nuclear factor kappa-B (NF-κB) was down-regulated with reduced inflammatory factors; meanwhile, the expression of nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) signaling was aggrandized. Conclusion These results suggest that SPJs treatment can improve age-associated renal fibrosis by inhibiting TGF-β1/Smad, NFκB signaling pathways and activating Nrf2-ARE signaling pathways and that SPJs can be a potentially valuable anti-renal fibrosis drug.
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the preventive effect of total saponins from Panax japonicus on inflammation and insulin resistance in adipose tissue of mice induced by a high fat diet
Journal of Functional Foods, 2021Co-Authors: Yue Shi, Changcheng Zhang, Ding Yuan, Chaoqi Liu, Zhengtai Liu, Liyue Gai, Yan Gao, Gang Zhou, Chengfu YuanAbstract:Abstract We aimed to investigate the effects of total saponins from Panax japonicus (TSPJ) on adipocyte inflammation and insulin resistance induced by a high-fat diet (HFD). Moreover, its underlying mechanism was further explored. In vivo, we found that TSPJ inhibited the activation of NF-κB and increase the transcription of p-AKT, leading to reduced inflammation and improved sensitivity of adipocytes to insulin. In vitro evaluation revealed that palmitic acid (PA) induced inflammation by activating the NF-κB pathway, and triggered insulin resistance by affecting the expression of p-AKT in adipocytes. Treatment with 30 mg/kg and 90 mg/kg TSJP in animals and pre-treatment with 25 μg/mL and 50 μg/mL TSJP in 3T3-L1 could inhibit inflammation and insulin resistance induced by HFD and PA. Our study showed that TSPJ inhibited adipocyte inflammation by inhibiting the NF-κB pathway. Besides, TSPJ could also affect the expression of p-AKT to increase insulin sensitivity in adipocytes via targeting AMPK.
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saponins of Panax japonicus confer neuroprotection against brain aging through mitochondrial related oxidative stress and autophagy in rats
Current Pharmaceutical Biotechnology, 2020Co-Authors: Jingzhi Wan, Changcheng Zhang, Haixia Zhao, Lili Deng, Zhiyong Zhou, Chaoqi Liu, Yaoyan Dun, Rui Wang, Chengfu Yuan, Ding YuanAbstract:Background Oxidative stress and mitochondrial dysfunction play a vital role in the pathogenesis of brain aging. Saponins from Panax japonicus (SPJ) have attracted much attention for their potential to attenuate age-related oxidative stress as the main ingredient in rhizomes of Panax japonicus. Objective This study aimed to investigate the neuroprotective effects of SPJ on natural aging rats as well as the underlying mechanisms regarding oxidative stress and mitochondrial pathway. Methods Sprague-Dawley rats were divided into control groups (3-, 9-, 15- and 24-month old groups) and SPJ-treated groups. For SPJ-treated groups, SPJ were orally administrated to 18-month old rats at doses of 10 mg/kg, 30 mg/kg and 60 mg/kg once daily. Control groups were given the same volume of saline. After the treatment with SPJ or saline for six months, the cortex and hippocampus were rapidly harvested and deposited at -80°C after the rats were decapitated under anesthesia. The neuroprotective effects of SPJ were estimated by histopathological observation, TUNEL detection, biochemical determination and western blotting. Results SPJ improved pathomorphological changes in neuronal cells and decreased apoptosis in the cortex and hippocampus of aging rats, increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), Na+/K+-ATPase, Ca2+-ATPase and Ca2+/Mg2+-ATPase whereas, decreased malondialdehyde (MDA) contents in the cortex of aging rats. Furthermore, the SPJ increased silent mating type information regulation 2 homolog-1 (SIRT1) protein expression, decreased acetylated level of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in the cortex and hippocampus of aging rats, and reversed the aging-induced decline of Forkhead box O3 (Foxo3a), Superoxide Dismutase 2 (SOD2), microtubule-associated protein light chain 3 (LC3II) and Beclin1 levels in the cortex and hippocampus. Conclusion Our data showed that SPJ conferred neuroprotection partly through the regulation of oxidative stress and mitochondria-related pathways in aging rats.
