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Mei Gao - One of the best experts on this subject based on the ideXlab platform.

  • Pinocembrin attenuates blood-brain barrier injury induced by global cerebral ischemia-reperfusion in rats
    Brain research, 2011
    Co-Authors: Fanrui Meng, Mei Gao, Rui Liu, Yue-hua Wang, Zhao-hong Xuan, Jialin Sun, Fan Yang
    Abstract:

    Blood-brain barrier (BBB) disruption is a major consequence of cerebral ischemia/reperfusion. Several studies have reported the neuroprotection of Pinocembrin on cerebral ischemia in vivo and in vitro, but the effects of Pinocembrin on BBB and its underlying mechanisms are not clear. In this study, we investigated the effects of Pinocembrin on BBB functions in the global cerebral ischemia/reperfusion (GCI/R) model in rats. Neurological scores and brain edema were evaluated. BBB permeability was assessed by detecting the concentrations of Evan's blue (EB) and fluorescein sodium (NaF) in brain tissue. The pathological changes of BBB ultrastructure were observed by transmission electron microscopy. Cerebral blood flow (CBF) was measured by laser Doppler flowmetry. The effects of Pinocembrin on primary cultured rat cerebral microvascular endothelial cells (RCMECs) against oxygen-glucose deprivation/reoxygenation (OGD/R) were also investigated. The results showed Pinocembrin decreased neurological score and lessened brain edema induced by GCI/R. Pinocembrin also reduced the concentrations of EB and NaF in brain tissue of the GCI/R rats. And Pinocembrin alleviated the ultrastructural changes of cerebral microvessels, astrocyte end-feet and neurons, and improved CBF in the GCI/R rats. In addition, Pinocembrin increased the viability and mitochondrial membrane potential of cultured RCMECs induced by OGD/R. In conclusion, these data demonstrate that Pinocembrin alleviates blood-brain barrier injury induced by GCI/R in rats.

  • the characteristics of therapeutic effect of Pinocembrin in transient global brain ischemia reperfusion rats
    Life Sciences, 2011
    Co-Authors: Lili Shi, Mei Gao, Bainian Chen, Hengai Zhang, Li Wang
    Abstract:

    Abstract Aims The therapeutic effect of Pinocembrin, together with the therapeutic time window, in the transient global cerebral ischemia/reperfusion (I/R) rats was investigated. Main methods Adult male Sprague–Dawley rats were subjected to global cerebral ischemia for 20 min by four-vessel occlusion. Pinocembrin (1 and 5 mg/kg) was administrated intravenously 30 min before ischemia and 30 min, 2 h, 6 h after reperfusion, respectively. Neurological scores, brain edema and histological examination by Nissl staining were employed to assess the neuronal injury after ischemia and the neuroprotection by Pinocembrin. The activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and the content of malondialdehyde (MDA) in brain tissue were tested by colorimetric assays. Alterations of neurotransmitters were determined by a high performance liquid chromatography–electrochemical method. Key findings Pinocembrin significantly ameliorated neurological deficits and brain edema, and alleviated the degree of hippocampal neuronal loss at 24 h after global cerebral I/R with a broad therapeutic time window. It was found that treatment with Pinocembrin reduced the compensatory increase of SOD activity and decreased the MDA level and MPO activity in a dose-dependent manner. The metabolic balance between excitatory and inhibitory amino acids was modulated by Pinocembrin treatment. Significance These findings suggest that Pinocembrin provides neuroprotection against global cerebral ischemic injury with a wide therapeutic time window, which may be attributed to its antioxidative, antiinflammatory and antiexcitotoxic effects.

  • The characteristics of therapeutic effect of Pinocembrin in transient global brain ischemia/reperfusion rats.
    Life sciences, 2011
    Co-Authors: Lili Shi, Mei Gao, Bainian Chen, Hengai Zhang, Li Wang
    Abstract:

    The therapeutic effect of Pinocembrin, together with the therapeutic time window, in the transient global cerebral ischemia/reperfusion (I/R) rats was investigated. Adult male Sprague-Dawley rats were subjected to global cerebral ischemia for 20 min by four-vessel occlusion. Pinocembrin (1 and 5mg/kg) was administrated intravenously 30 min before ischemia and 30 min, 2h, 6h after reperfusion, respectively. Neurological scores, brain edema and histological examination by Nissl staining were employed to assess the neuronal injury after ischemia and the neuroprotection by Pinocembrin. The activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and the content of malondialdehyde (MDA) in brain tissue were tested by colorimetric assays. Alterations of neurotransmitters were determined by a high performance liquid chromatography-electrochemical method. Pinocembrin significantly ameliorated neurological deficits and brain edema, and alleviated the degree of hippocampal neuronal loss at 24h after global cerebral I/R with a broad therapeutic time window. It was found that treatment with Pinocembrin reduced the compensatory increase of SOD activity and decreased the MDA level and MPO activity in a dose-dependent manner. The metabolic balance between excitatory and inhibitory amino acids was modulated by Pinocembrin treatment. These findings suggest that Pinocembrin provides neuroprotection against global cerebral ischemic injury with a wide therapeutic time window, which may be attributed to its antioxidative, antiinflammatory and antiexcitotoxic effects. Copyright © 2011 Elsevier B.V. All rights reserved.

  • The characteristics of therapeutic effect of Pinocembrin in transient global brain ischemia/reperfusion rats.
    Life Sciences, 2011
    Co-Authors: Lili Shi, Mei Gao, Bainian Chen, Hengai Zhang, Li Wang
    Abstract:

    Abstract Aims The therapeutic effect of Pinocembrin, together with the therapeutic time window, in the transient global cerebral ischemia/reperfusion (I/R) rats was investigated. Main methods Adult male Sprague–Dawley rats were subjected to global cerebral ischemia for 20 min by four-vessel occlusion. Pinocembrin (1 and 5 mg/kg) was administrated intravenously 30 min before ischemia and 30 min, 2 h, 6 h after reperfusion, respectively. Neurological scores, brain edema and histological examination by Nissl staining were employed to assess the neuronal injury after ischemia and the neuroprotection by Pinocembrin. The activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and the content of malondialdehyde (MDA) in brain tissue were tested by colorimetric assays. Alterations of neurotransmitters were determined by a high performance liquid chromatography–electrochemical method. Key findings Pinocembrin significantly ameliorated neurological deficits and brain edema, and alleviated the degree of hippocampal neuronal loss at 24 h after global cerebral I/R with a broad therapeutic time window. It was found that treatment with Pinocembrin reduced the compensatory increase of SOD activity and decreased the MDA level and MPO activity in a dose-dependent manner. The metabolic balance between excitatory and inhibitory amino acids was modulated by Pinocembrin treatment. Significance These findings suggest that Pinocembrin provides neuroprotection against global cerebral ischemic injury with a wide therapeutic time window, which may be attributed to its antioxidative, antiinflammatory and antiexcitotoxic effects.

  • Effect of Pinocembrin on brain mitochondrial respiratory function
    Yao xue xue bao = Acta pharmaceutica Sinica, 2011
    Co-Authors: Lili Shi, Mei Gao, Bainian Chen, Zhao-hong Xuan, Guifen Qiang, Hengai Zhang, Qiao-yun Wang
    Abstract:

    There are growing evidences that Pinocembrin has better neuroprotective effect. In the present study, the effect of Pinocembrin on mitochondrial respiratory function was evaluated in global brain ischemia/ reperfusion (4-vessel occlusion, 4-VO) rats. The results showed that Pinocembrin improved the respiratory activity of 4-VO brain mitochondria, through increasing ADP/O, state 3 respiration state (V3), respiration control rate index (RCI) and oxidative phosphorylation rate (OPR). And then, the effect of Pinocembrin on brain mitochondria was verified in vitro. The results showed that Pinocembrin increased ADP/O, state 3 respiration state, respiration control rate index, oxidative phosphorylation rate in NADH/FADH2 dependent respiratory chain and decreased state 4 respiration state (V4) in NADH dependent respiratory chain. Pinocembrin improved ATP content in brain mitochondria in vitro and in SH-SY5Y cells.

Yuan-wei Shih - One of the best experts on this subject based on the ideXlab platform.

  • Pinocembrin suppresses TGF-β1-induced epithelial-mesenchymal transition and metastasis of human Y-79 retinoblastoma cells through inactivating αvβ3 integrin/FAK/p38α signaling pathway
    Cell & Bioscience, 2014
    Co-Authors: Kun-shiang Chen, Chi Sheng Chien, Yuan-wei Shih
    Abstract:

    Background Pinocembrin is the most abundant flavonoid in propolis. In this study, we investigated the antimetastatic effect of Pinocembrin on TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of human Y-79 retinoblastoma cells. Results Firstly, the results showed that Pinocembrin significantly suppresses the TGF-β1-induced abilities of the invasion and migration of Y-79 cells under non-cytotoxic concentration. Pinocembrin decreased TGF-β1-induced expression of vimentin, N-cadherin, αv and β3 integrin in Y-79 cells. Molecular data also showed Pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38α signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-β1. Next, Pinocembrin also strongly inhibited the degradation of inhibitor of kappaBα (IκBα) and the nuclear levels of nuclear factor kappa B (NF-κB). Also, a dose-dependent inhibition on the binding ability of NF-κB was further observed under Pinocembrin treatment. Conclusions Presented results indicated that Pinocembrin inhibits TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of Y-79 cells by inactivating the αvβ3 integrin/FAK/p38α signaling pathway. Thus, our findings point to the anticancer potential of Pinocembrin against retinoblastoma cells.

  • Pinocembrin suppresses TGF-β1-induced epithelial-mesenchymal transition and metastasis of human Y-79 retinoblastoma cells through inactivating αvβ3 integrin/FAK/p38α signaling pathway
    Cell & bioscience, 2014
    Co-Authors: Kun-shiang Chen, Chi Sheng Chien, Ming-der Shi, Yuan-wei Shih
    Abstract:

    Pinocembrin is the most abundant flavonoid in propolis. In this study, we investigated the antimetastatic effect of Pinocembrin on TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of human Y-79 retinoblastoma cells. Firstly, the results showed that Pinocembrin significantly suppresses the TGF-β1-induced abilities of the invasion and migration of Y-79 cells under non-cytotoxic concentration. Pinocembrin decreased TGF-β1-induced expression of vimentin, N-cadherin, αv and β3 integrin in Y-79 cells. Molecular data also showed Pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38α signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-β1. Next, Pinocembrin also strongly inhibited the degradation of inhibitor of kappaBα (IκBα) and the nuclear levels of nuclear factor kappa B (NF-κB). Also, a dose-dependent inhibition on the binding ability of NF-κB was further observed under Pinocembrin treatment. Presented results indicated that Pinocembrin inhibits TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of Y-79 cells by inactivating the αvβ3 integrin/FAK/p38α signaling pathway. Thus, our findings point to the anticancer potential of Pinocembrin against retinoblastoma cells.

Wei Dou - One of the best experts on this subject based on the ideXlab platform.

  • Pinocembrin alleviates ulcerative colitis in mice via regulating gut microbiota suppressing tlr4 md2 nf κb pathway and promoting intestinal barrier
    Bioscience Reports, 2020
    Co-Authors: Bei Yue, Junyu Ren, Xiaoping Luo, Yijing Ren, Jing Zhang, Sridhar Mani, Zhengtao Wang, Wei Dou
    Abstract:

    Pinocembrin, a plant-derived flavonoid, has a variety of pharmacological activities, including anti-infection, anti-cancer, anti-inflammation, cardiovascular protection, etc. However, the mechanism of Pinocembrin on the anti-colitis efficacy remains elusive and needs further investigation. Here, we reported that Pinocembrin eased the severity of dextran sulfate sodium (DSS)-induced colitis in mice by suppressing the abnormal activation of toll-like receptor 4 (TLR4) / nuclear factor-kappa B (NF-κB) signal pathway in vivo. In addition, the gut microbiota was disordered in DSS colitis mice, which was associated with a significant decrease in microbiota diversity and a great shift in bacteria profiles; however, Pinocembrin treatment improved the imbalance of gut microbiota and made it similar to that in normal mice. On the other hand, in vitro, Pinocembrin down-regulated the TLR4/NF-κB signaling cascades in lipopolysaccharide (LPS)-stimulated macrophages. At the upstream level, Pinocembrin competitively inhibited the binding of LPS to myeloid differentiation protein 2 (MD2), thereby blocking the formation of receptor multimer TLR4/MD2·LPS. Furthermore, Pinocembrin dose-dependently promoted the expression of tight junction proteins (ZO-1, Claudin-1, Occludin and JAM-A) in Caco-2 cells. In conclusion, our work presented evidence that Pinocembrin attenuated DSS-induced colitis in mouse, at least in part, via regulating intestinal microbiota, inhibiting the over-activation of TLR4/MD2/NF-κB signaling pathway, and improving the barriers of intestine.

  • Pinocembrin alleviates ulcerative colitis in mice via regulating gut microbiota, suppressing TLR4/MD2/NF-κB pathway and promoting intestinal barrier.
    Bioscience reports, 2020
    Co-Authors: Bei Yue, Junyu Ren, Xiaoping Luo, Yijing Ren, Jing Zhang, Sridhar Mani, Zhengtao Wang, Wei Dou
    Abstract:

    Pinocembrin, a plant-derived flavonoid, has a variety of pharmacological activities, including anti-infection, anti-cancer, anti-inflammation, cardiovascular protection, etc. However, the mechanism of Pinocembrin on the anti-colitis efficacy remains elusive and needs further investigation. Here, we reported that Pinocembrin eased the severity of dextran sulfate sodium (DSS)-induced colitis in mice by suppressing the abnormal activation of toll-like receptor 4 (TLR4) / nuclear factor-kappa B (NF-κB) signal pathway in vivo. In addition, the gut microbiota was disordered in DSS colitis mice, which was associated with a significant decrease in microbiota diversity and a great shift in bacteria profiles; however, Pinocembrin treatment improved the imbalance of gut microbiota and made it similar to that in normal mice. On the other hand, in vitro, Pinocembrin down-regulated the TLR4/NF-κB signaling cascades in lipopolysaccharide (LPS)-stimulated macrophages. At the upstream level, Pinocembrin competitively inhibited the binding of LPS to myeloid differentiation protein 2 (MD2), thereby blocking the formation of receptor multimer TLR4/MD2·LPS. Furthermore, Pinocembrin dose-dependently promoted the expression of tight junction proteins (ZO-1, Claudin-1, Occludin and JAM-A) in Caco-2 cells. In conclusion, our work presented evidence that Pinocembrin attenuated DSS-induced colitis in mouse, at least in part, via regulating intestinal microbiota, inhibiting the over-activation of TLR4/MD2/NF-κB signaling pathway, and improving the barriers of intestine.

Li Wang - One of the best experts on this subject based on the ideXlab platform.

  • the characteristics of therapeutic effect of Pinocembrin in transient global brain ischemia reperfusion rats
    Life Sciences, 2011
    Co-Authors: Lili Shi, Mei Gao, Bainian Chen, Hengai Zhang, Li Wang
    Abstract:

    Abstract Aims The therapeutic effect of Pinocembrin, together with the therapeutic time window, in the transient global cerebral ischemia/reperfusion (I/R) rats was investigated. Main methods Adult male Sprague–Dawley rats were subjected to global cerebral ischemia for 20 min by four-vessel occlusion. Pinocembrin (1 and 5 mg/kg) was administrated intravenously 30 min before ischemia and 30 min, 2 h, 6 h after reperfusion, respectively. Neurological scores, brain edema and histological examination by Nissl staining were employed to assess the neuronal injury after ischemia and the neuroprotection by Pinocembrin. The activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and the content of malondialdehyde (MDA) in brain tissue were tested by colorimetric assays. Alterations of neurotransmitters were determined by a high performance liquid chromatography–electrochemical method. Key findings Pinocembrin significantly ameliorated neurological deficits and brain edema, and alleviated the degree of hippocampal neuronal loss at 24 h after global cerebral I/R with a broad therapeutic time window. It was found that treatment with Pinocembrin reduced the compensatory increase of SOD activity and decreased the MDA level and MPO activity in a dose-dependent manner. The metabolic balance between excitatory and inhibitory amino acids was modulated by Pinocembrin treatment. Significance These findings suggest that Pinocembrin provides neuroprotection against global cerebral ischemic injury with a wide therapeutic time window, which may be attributed to its antioxidative, antiinflammatory and antiexcitotoxic effects.

  • The characteristics of therapeutic effect of Pinocembrin in transient global brain ischemia/reperfusion rats.
    Life sciences, 2011
    Co-Authors: Lili Shi, Mei Gao, Bainian Chen, Hengai Zhang, Li Wang
    Abstract:

    The therapeutic effect of Pinocembrin, together with the therapeutic time window, in the transient global cerebral ischemia/reperfusion (I/R) rats was investigated. Adult male Sprague-Dawley rats were subjected to global cerebral ischemia for 20 min by four-vessel occlusion. Pinocembrin (1 and 5mg/kg) was administrated intravenously 30 min before ischemia and 30 min, 2h, 6h after reperfusion, respectively. Neurological scores, brain edema and histological examination by Nissl staining were employed to assess the neuronal injury after ischemia and the neuroprotection by Pinocembrin. The activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and the content of malondialdehyde (MDA) in brain tissue were tested by colorimetric assays. Alterations of neurotransmitters were determined by a high performance liquid chromatography-electrochemical method. Pinocembrin significantly ameliorated neurological deficits and brain edema, and alleviated the degree of hippocampal neuronal loss at 24h after global cerebral I/R with a broad therapeutic time window. It was found that treatment with Pinocembrin reduced the compensatory increase of SOD activity and decreased the MDA level and MPO activity in a dose-dependent manner. The metabolic balance between excitatory and inhibitory amino acids was modulated by Pinocembrin treatment. These findings suggest that Pinocembrin provides neuroprotection against global cerebral ischemic injury with a wide therapeutic time window, which may be attributed to its antioxidative, antiinflammatory and antiexcitotoxic effects. Copyright © 2011 Elsevier B.V. All rights reserved.

  • The characteristics of therapeutic effect of Pinocembrin in transient global brain ischemia/reperfusion rats.
    Life Sciences, 2011
    Co-Authors: Lili Shi, Mei Gao, Bainian Chen, Hengai Zhang, Li Wang
    Abstract:

    Abstract Aims The therapeutic effect of Pinocembrin, together with the therapeutic time window, in the transient global cerebral ischemia/reperfusion (I/R) rats was investigated. Main methods Adult male Sprague–Dawley rats were subjected to global cerebral ischemia for 20 min by four-vessel occlusion. Pinocembrin (1 and 5 mg/kg) was administrated intravenously 30 min before ischemia and 30 min, 2 h, 6 h after reperfusion, respectively. Neurological scores, brain edema and histological examination by Nissl staining were employed to assess the neuronal injury after ischemia and the neuroprotection by Pinocembrin. The activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and the content of malondialdehyde (MDA) in brain tissue were tested by colorimetric assays. Alterations of neurotransmitters were determined by a high performance liquid chromatography–electrochemical method. Key findings Pinocembrin significantly ameliorated neurological deficits and brain edema, and alleviated the degree of hippocampal neuronal loss at 24 h after global cerebral I/R with a broad therapeutic time window. It was found that treatment with Pinocembrin reduced the compensatory increase of SOD activity and decreased the MDA level and MPO activity in a dose-dependent manner. The metabolic balance between excitatory and inhibitory amino acids was modulated by Pinocembrin treatment. Significance These findings suggest that Pinocembrin provides neuroprotection against global cerebral ischemic injury with a wide therapeutic time window, which may be attributed to its antioxidative, antiinflammatory and antiexcitotoxic effects.

Kun-shiang Chen - One of the best experts on this subject based on the ideXlab platform.

  • Pinocembrin suppresses TGF-β1-induced epithelial-mesenchymal transition and metastasis of human Y-79 retinoblastoma cells through inactivating αvβ3 integrin/FAK/p38α signaling pathway
    Cell & Bioscience, 2014
    Co-Authors: Kun-shiang Chen, Chi Sheng Chien, Yuan-wei Shih
    Abstract:

    Background Pinocembrin is the most abundant flavonoid in propolis. In this study, we investigated the antimetastatic effect of Pinocembrin on TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of human Y-79 retinoblastoma cells. Results Firstly, the results showed that Pinocembrin significantly suppresses the TGF-β1-induced abilities of the invasion and migration of Y-79 cells under non-cytotoxic concentration. Pinocembrin decreased TGF-β1-induced expression of vimentin, N-cadherin, αv and β3 integrin in Y-79 cells. Molecular data also showed Pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38α signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-β1. Next, Pinocembrin also strongly inhibited the degradation of inhibitor of kappaBα (IκBα) and the nuclear levels of nuclear factor kappa B (NF-κB). Also, a dose-dependent inhibition on the binding ability of NF-κB was further observed under Pinocembrin treatment. Conclusions Presented results indicated that Pinocembrin inhibits TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of Y-79 cells by inactivating the αvβ3 integrin/FAK/p38α signaling pathway. Thus, our findings point to the anticancer potential of Pinocembrin against retinoblastoma cells.

  • Pinocembrin suppresses TGF-β1-induced epithelial-mesenchymal transition and metastasis of human Y-79 retinoblastoma cells through inactivating αvβ3 integrin/FAK/p38α signaling pathway
    Cell & bioscience, 2014
    Co-Authors: Kun-shiang Chen, Chi Sheng Chien, Ming-der Shi, Yuan-wei Shih
    Abstract:

    Pinocembrin is the most abundant flavonoid in propolis. In this study, we investigated the antimetastatic effect of Pinocembrin on TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of human Y-79 retinoblastoma cells. Firstly, the results showed that Pinocembrin significantly suppresses the TGF-β1-induced abilities of the invasion and migration of Y-79 cells under non-cytotoxic concentration. Pinocembrin decreased TGF-β1-induced expression of vimentin, N-cadherin, αv and β3 integrin in Y-79 cells. Molecular data also showed Pinocembrin inhibits the activation of focal adhesion kinase (FAK) and p38α signal involved in the downregulation of enzyme activities, protein and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/-9) induced by TGF-β1. Next, Pinocembrin also strongly inhibited the degradation of inhibitor of kappaBα (IκBα) and the nuclear levels of nuclear factor kappa B (NF-κB). Also, a dose-dependent inhibition on the binding ability of NF-κB was further observed under Pinocembrin treatment. Presented results indicated that Pinocembrin inhibits TGF-β1-induced epithelial-mesenchymal transition (EMT) and metastasis of Y-79 cells by inactivating the αvβ3 integrin/FAK/p38α signaling pathway. Thus, our findings point to the anticancer potential of Pinocembrin against retinoblastoma cells.