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Junqing Yang - One of the best experts on this subject based on the ideXlab platform.

  • treatment with either cox 2 inhibitor or 5 lox inhibitor causes no compensation between cox 2 pathway and 5 lox pathway in chronic Aluminum Overload induced liver injury in rats
    Fundamental & Clinical Pharmacology, 2019
    Co-Authors: Hui Xia, Hong Wang, Yongming Wang, Yang Yang, Jiahua Zhang, Zhihao Chen, Junqing Yang
    Abstract:

    This study was designed to observe the compensation between cyclooxygenase-2 pathway and 5-lipoxygenase pathway in chronic Aluminum Overload-induced liver injury rats. A rat hepatic injury model of chronic Aluminum injury was established by the intragastric administration of Aluminum gluconate (Al3 + 200 mg/kg per day, 5 days a week for 20 weeks). The COX-2 inhibitor [meloxicam (1 mg/kg)] and 5-LOX inhibitor [caffeic acid (30 mg/kg)] were intragastrically administered 1 h after Aluminum administration. The histopathology was detected by hematoxylin-eosin staining. A series of biochemical indicators were measured with biochemistry assay or ELISAs. The expressions of COX-2 and 5-LOX were measured by immunohistochemistry. Our experimental results showed that Aluminum Overload caused a significant damage to the liver and also significantly increased the expressions of COX-2, 5-LOX and the levels of inflammation and oxidative stress. The administration of meloxicam and caffeic acid significantly protected livers against histopathological injury, significantly decreased plasma ALT, AST, and ALP levels, significantly decreased TNF-α, IL-6, IL-1β levels, and oxidative stress. However, the administration of caffeic acid did not significantly increase the expression of COX-2 compared with the model group. On the other hand, the administration of meloxicam also did not significantly increase the expression of 5-LOX compared with the model group. Our results indicate that there is no compensation between COX-2 pathway and 5-LOX pathway by inhibiting either COX-2 or 5-LOX in chronic Aluminum Overload-induced liver injury rat.

  • cysltr1 blockage ameliorates liver injury caused by Aluminum Overload via pi3k akt mtor mediated autophagy activation in vivo and in vitro
    Molecular Pharmaceutics, 2018
    Co-Authors: Junqing Yang, Hui Xia, Yang Yang, Jiahua Zhang, Zhihao Chen, Ying Luo, Lu Yang, Dongzhi Ran, Hong Wang
    Abstract:

    Aluminum (Al) is a trivalent cation that can accumulate in animal organs, especially in the liver. We previously demonstrated that Al-Overload could induce liver morphologic aberrations and dysfunction. However, the molecular mechanism underlying liver injury caused by Al-Overload still remains unknown. In the present study, we investigated the relationship between leukotrienes receptors and the PI3K/AKT/mTOR pathway in Al-induced liver injury in vivo and in vitro. We demonstrated that Al-Overload significantly increased the protein expression levels of CysLTR1, PI3K, AKT, mTOR, and p62, while significantly decreasing the LC3BII protein levels in rat liver; thus, suggesting that the autophagy process was inhibited in Al-Overloaded rat liver. In addition, MK-571, an inhibitor of CysLTR1, effectively protected the human hepatocyte L02 cells against injury caused by Al exposure. Moreover, CysLTR1 blockage could significantly down-regulate the PI3K/AKT/mTOR pathway and activate autophagy. The effect of MK-571...

  • misoprostol reverse hippocampal neuron cyclooxygenase 2 downstream signaling imbalance in Aluminum Overload rats
    Current Alzheimer Research, 2016
    Co-Authors: Yuanxin Guo, Wenjuan Lei, Jianfeng Wang, Yuling Wei, Junqing Yang
    Abstract:

    Although COX-2 inhibition in animal models of neurodegenerative diseases has shown neuroprotection, recent studies have revealed some serious side effects (ulcers, bleeding, fatal cerebrovascular diseases etc.) and the limited benefits of COX-2 inhibitors. A more focused approach is necessary to explore the therapeutic effect of the COX downstream signaling pathway in neurological research. The aim of this study was to explore the alterations of the PGES-PGE 2 -EP signal pathway and the effect of misoprostol on neurodegeneration by chronic Aluminum-Overload in rats. Adult rats were treated by intragastric administration of Aluminum gluconate. The PGE 2 content and expression of PGES and EPs in the hippocampi of rats were detected using ELISA, q-PCR and Western blot analysis, respectively. The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in the rat hippocampi were also detected. The misoprostol treatment dose-dependently improved spatial learning and memory function as well as healing after hippocampal neuron damage induced by chronic Aluminum-Overload in rats. Meanwhile, the administration of misoprostol resulted in a decrease in the PGE2 level and down-regulation of the mPGES-1, EP 2 and EP 4 expression levels, while there was a dosedependent up-regulation of EP3 expression. These results suggest that misoprostol possesses a neuroprotective property, and the mechanism involves affecting the EP3 level and reducing the endogenous production of PGE 2 through a negative feedback mechanism, increasing the EP 3 expression level, decreasing the EP 2 and EP 4 expression levels, and rebuilding the mPGES-1-PGE 2 -EP 1-4 signal pathway balance. In this way, misoprostol has a counteractive effect on oxidant stress and inflammation in the central nervous system. The PGES-PGE2-EPs signaling pathway is a potential therapeutic strategy for treating neurodegeneration in patients.

  • 5 lipoxygenase activation is involved in the mechanisms of chronic hepatic injury in a rat model of chronic Aluminum Overload exposure
    Toxicology and Applied Pharmacology, 2016
    Co-Authors: Shaoshan Mai, Hong Wang, Yang Yang, Ying Luo, Shengnan Kuang, Xiaoyan Tian, Junqing Yang
    Abstract:

    We previously confirmed that rats Overloaded with Aluminum exhibited hepatic function damage and increased susceptibility to hepatic inflammation. However, the mechanism of liver toxicity by chronic Aluminum Overload is poorly understood. In this study, we investigated changes in the 5-lipoxygenase (5-LO) signaling pathway and its effect on liver injury in Aluminum-Overloaded rats. A rat hepatic injury model of chronic Aluminum injury was established via the intragastric administration of Aluminum gluconate (Al(3+) 200mg/kg per day, 5days a week for 20weeks). The 5-LO inhibitor, caffeic acid (10 and 30mg/kg), was intragastrically administered 1h after Aluminum administration. Hematoxylin and eosin staining was used to visualize pathological changes in rat liver tissue. A series of biochemical indicators were measured with biochemistry assay or ELISAs. Immunochemistry and RT-PCR methods were used to detect 5-LO protein and mRNA expression in the liver, respectively. Caffeic acid administration protected livers against histopathological injury, decreased plasma ALT, AST, and ALP levels, decreased TNF-α, IL-6, IL-1β and LTs levels, increased the reactive oxygen species content, and down-regulated the mRNA and protein expressions of 5-LO in Aluminum Overloaded rats. Our results indicate that 5-lipoxygenase activation is mechanistically involved in chronic hepatic injury in a rat model of chronic Aluminum Overload exposure and that the 5-LO signaling pathway, which associated with inflammation and oxidative stress, is a potential therapeutic target for chronic non-infection liver diseases.

  • effect of the pgd2 dp signaling pathway on primary cultured rat hippocampal neuron injury caused by Aluminum Overload
    Scientific Reports, 2016
    Co-Authors: Qunfang Yang, Yuling Wei, Yang Yang, Shaoshan Mai, Ying Luo, Shengnan Kuang, Xiaoyan Tian, Guojuan Liang, Junqing Yang
    Abstract:

    In the present study, the agonists and antagonists of DP receptor were used to examine whether the PGD2-DP signaling pathway affects neuronal function. Primary cultured hippocampal neuron was prepared and treated with Aluminum maltolate (100 μM) to establish the neuronal damage model. PGD2 and cAMP content was detected by ELISA. L-PGDS and DPs mRNA and protein expression were measured by RT-PCR and Western blotting, respectively. The aluminium-load neuron was treated with the DP1 agonist BW245C, the DP1 antagonist BWA868C, the DP2 agonist DK-PGD2, and the DP2 antagonist CAY10471, respectively. Neuronal pathomorphology was observed using H-E staining. The cell viability and the lactate dehydrogenase leakage rates of neurons were measured with MTT and LDH kit, respectively. Ca(2+) level was detected by Fluo-3/AM. In the model group, the MTT values obviously decreased; LDH leakage rates and PGD2 content increased significantly; L-PGDS, DP1 mRNA and protein expressions increased, and DP2 level decreased. BW245C reduced the Ca(2+) fluorescence intensity and protected the neurons. DK-PGD2 increased the intensity of Ca(2+) fluorescence, while CAY10471 had the opposite effect. In conclusion, contrary to the effect of DP2, the PGD2-DP1 signaling pathway protects against the primary cultured rat hippocampal neuronal injury caused by Aluminum Overload.

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

  • treatment with either cox 2 inhibitor or 5 lox inhibitor causes no compensation between cox 2 pathway and 5 lox pathway in chronic Aluminum Overload induced liver injury in rats
    Fundamental & Clinical Pharmacology, 2019
    Co-Authors: Hui Xia, Hong Wang, Yongming Wang, Yang Yang, Jiahua Zhang, Zhihao Chen, Junqing Yang
    Abstract:

    This study was designed to observe the compensation between cyclooxygenase-2 pathway and 5-lipoxygenase pathway in chronic Aluminum Overload-induced liver injury rats. A rat hepatic injury model of chronic Aluminum injury was established by the intragastric administration of Aluminum gluconate (Al3 + 200 mg/kg per day, 5 days a week for 20 weeks). The COX-2 inhibitor [meloxicam (1 mg/kg)] and 5-LOX inhibitor [caffeic acid (30 mg/kg)] were intragastrically administered 1 h after Aluminum administration. The histopathology was detected by hematoxylin-eosin staining. A series of biochemical indicators were measured with biochemistry assay or ELISAs. The expressions of COX-2 and 5-LOX were measured by immunohistochemistry. Our experimental results showed that Aluminum Overload caused a significant damage to the liver and also significantly increased the expressions of COX-2, 5-LOX and the levels of inflammation and oxidative stress. The administration of meloxicam and caffeic acid significantly protected livers against histopathological injury, significantly decreased plasma ALT, AST, and ALP levels, significantly decreased TNF-α, IL-6, IL-1β levels, and oxidative stress. However, the administration of caffeic acid did not significantly increase the expression of COX-2 compared with the model group. On the other hand, the administration of meloxicam also did not significantly increase the expression of 5-LOX compared with the model group. Our results indicate that there is no compensation between COX-2 pathway and 5-LOX pathway by inhibiting either COX-2 or 5-LOX in chronic Aluminum Overload-induced liver injury rat.

  • cysltr1 blockage ameliorates liver injury caused by Aluminum Overload via pi3k akt mtor mediated autophagy activation in vivo and in vitro
    Molecular Pharmaceutics, 2018
    Co-Authors: Junqing Yang, Hui Xia, Yang Yang, Jiahua Zhang, Zhihao Chen, Ying Luo, Lu Yang, Dongzhi Ran, Hong Wang
    Abstract:

    Aluminum (Al) is a trivalent cation that can accumulate in animal organs, especially in the liver. We previously demonstrated that Al-Overload could induce liver morphologic aberrations and dysfunction. However, the molecular mechanism underlying liver injury caused by Al-Overload still remains unknown. In the present study, we investigated the relationship between leukotrienes receptors and the PI3K/AKT/mTOR pathway in Al-induced liver injury in vivo and in vitro. We demonstrated that Al-Overload significantly increased the protein expression levels of CysLTR1, PI3K, AKT, mTOR, and p62, while significantly decreasing the LC3BII protein levels in rat liver; thus, suggesting that the autophagy process was inhibited in Al-Overloaded rat liver. In addition, MK-571, an inhibitor of CysLTR1, effectively protected the human hepatocyte L02 cells against injury caused by Al exposure. Moreover, CysLTR1 blockage could significantly down-regulate the PI3K/AKT/mTOR pathway and activate autophagy. The effect of MK-571...

  • 5 lipoxygenase activation is involved in the mechanisms of chronic hepatic injury in a rat model of chronic Aluminum Overload exposure
    Toxicology and Applied Pharmacology, 2016
    Co-Authors: Shaoshan Mai, Hong Wang, Yang Yang, Ying Luo, Shengnan Kuang, Xiaoyan Tian, Junqing Yang
    Abstract:

    We previously confirmed that rats Overloaded with Aluminum exhibited hepatic function damage and increased susceptibility to hepatic inflammation. However, the mechanism of liver toxicity by chronic Aluminum Overload is poorly understood. In this study, we investigated changes in the 5-lipoxygenase (5-LO) signaling pathway and its effect on liver injury in Aluminum-Overloaded rats. A rat hepatic injury model of chronic Aluminum injury was established via the intragastric administration of Aluminum gluconate (Al(3+) 200mg/kg per day, 5days a week for 20weeks). The 5-LO inhibitor, caffeic acid (10 and 30mg/kg), was intragastrically administered 1h after Aluminum administration. Hematoxylin and eosin staining was used to visualize pathological changes in rat liver tissue. A series of biochemical indicators were measured with biochemistry assay or ELISAs. Immunochemistry and RT-PCR methods were used to detect 5-LO protein and mRNA expression in the liver, respectively. Caffeic acid administration protected livers against histopathological injury, decreased plasma ALT, AST, and ALP levels, decreased TNF-α, IL-6, IL-1β and LTs levels, increased the reactive oxygen species content, and down-regulated the mRNA and protein expressions of 5-LO in Aluminum Overloaded rats. Our results indicate that 5-lipoxygenase activation is mechanistically involved in chronic hepatic injury in a rat model of chronic Aluminum Overload exposure and that the 5-LO signaling pathway, which associated with inflammation and oxidative stress, is a potential therapeutic target for chronic non-infection liver diseases.

  • effect of the pgd2 dp signaling pathway on primary cultured rat hippocampal neuron injury caused by Aluminum Overload
    Scientific Reports, 2016
    Co-Authors: Qunfang Yang, Yuling Wei, Yang Yang, Shaoshan Mai, Ying Luo, Shengnan Kuang, Xiaoyan Tian, Guojuan Liang, Junqing Yang
    Abstract:

    In the present study, the agonists and antagonists of DP receptor were used to examine whether the PGD2-DP signaling pathway affects neuronal function. Primary cultured hippocampal neuron was prepared and treated with Aluminum maltolate (100 μM) to establish the neuronal damage model. PGD2 and cAMP content was detected by ELISA. L-PGDS and DPs mRNA and protein expression were measured by RT-PCR and Western blotting, respectively. The aluminium-load neuron was treated with the DP1 agonist BW245C, the DP1 antagonist BWA868C, the DP2 agonist DK-PGD2, and the DP2 antagonist CAY10471, respectively. Neuronal pathomorphology was observed using H-E staining. The cell viability and the lactate dehydrogenase leakage rates of neurons were measured with MTT and LDH kit, respectively. Ca(2+) level was detected by Fluo-3/AM. In the model group, the MTT values obviously decreased; LDH leakage rates and PGD2 content increased significantly; L-PGDS, DP1 mRNA and protein expressions increased, and DP2 level decreased. BW245C reduced the Ca(2+) fluorescence intensity and protected the neurons. DK-PGD2 increased the intensity of Ca(2+) fluorescence, while CAY10471 had the opposite effect. In conclusion, contrary to the effect of DP2, the PGD2-DP1 signaling pathway protects against the primary cultured rat hippocampal neuronal injury caused by Aluminum Overload.

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

  • treatment with either cox 2 inhibitor or 5 lox inhibitor causes no compensation between cox 2 pathway and 5 lox pathway in chronic Aluminum Overload induced liver injury in rats
    Fundamental & Clinical Pharmacology, 2019
    Co-Authors: Hui Xia, Hong Wang, Yongming Wang, Yang Yang, Jiahua Zhang, Zhihao Chen, Junqing Yang
    Abstract:

    This study was designed to observe the compensation between cyclooxygenase-2 pathway and 5-lipoxygenase pathway in chronic Aluminum Overload-induced liver injury rats. A rat hepatic injury model of chronic Aluminum injury was established by the intragastric administration of Aluminum gluconate (Al3 + 200 mg/kg per day, 5 days a week for 20 weeks). The COX-2 inhibitor [meloxicam (1 mg/kg)] and 5-LOX inhibitor [caffeic acid (30 mg/kg)] were intragastrically administered 1 h after Aluminum administration. The histopathology was detected by hematoxylin-eosin staining. A series of biochemical indicators were measured with biochemistry assay or ELISAs. The expressions of COX-2 and 5-LOX were measured by immunohistochemistry. Our experimental results showed that Aluminum Overload caused a significant damage to the liver and also significantly increased the expressions of COX-2, 5-LOX and the levels of inflammation and oxidative stress. The administration of meloxicam and caffeic acid significantly protected livers against histopathological injury, significantly decreased plasma ALT, AST, and ALP levels, significantly decreased TNF-α, IL-6, IL-1β levels, and oxidative stress. However, the administration of caffeic acid did not significantly increase the expression of COX-2 compared with the model group. On the other hand, the administration of meloxicam also did not significantly increase the expression of 5-LOX compared with the model group. Our results indicate that there is no compensation between COX-2 pathway and 5-LOX pathway by inhibiting either COX-2 or 5-LOX in chronic Aluminum Overload-induced liver injury rat.

  • cysltr1 blockage ameliorates liver injury caused by Aluminum Overload via pi3k akt mtor mediated autophagy activation in vivo and in vitro
    Molecular Pharmaceutics, 2018
    Co-Authors: Junqing Yang, Hui Xia, Yang Yang, Jiahua Zhang, Zhihao Chen, Ying Luo, Lu Yang, Dongzhi Ran, Hong Wang
    Abstract:

    Aluminum (Al) is a trivalent cation that can accumulate in animal organs, especially in the liver. We previously demonstrated that Al-Overload could induce liver morphologic aberrations and dysfunction. However, the molecular mechanism underlying liver injury caused by Al-Overload still remains unknown. In the present study, we investigated the relationship between leukotrienes receptors and the PI3K/AKT/mTOR pathway in Al-induced liver injury in vivo and in vitro. We demonstrated that Al-Overload significantly increased the protein expression levels of CysLTR1, PI3K, AKT, mTOR, and p62, while significantly decreasing the LC3BII protein levels in rat liver; thus, suggesting that the autophagy process was inhibited in Al-Overloaded rat liver. In addition, MK-571, an inhibitor of CysLTR1, effectively protected the human hepatocyte L02 cells against injury caused by Al exposure. Moreover, CysLTR1 blockage could significantly down-regulate the PI3K/AKT/mTOR pathway and activate autophagy. The effect of MK-571...

  • 5 lipoxygenase activation is involved in the mechanisms of chronic hepatic injury in a rat model of chronic Aluminum Overload exposure
    Toxicology and Applied Pharmacology, 2016
    Co-Authors: Shaoshan Mai, Hong Wang, Yang Yang, Ying Luo, Shengnan Kuang, Xiaoyan Tian, Junqing Yang
    Abstract:

    We previously confirmed that rats Overloaded with Aluminum exhibited hepatic function damage and increased susceptibility to hepatic inflammation. However, the mechanism of liver toxicity by chronic Aluminum Overload is poorly understood. In this study, we investigated changes in the 5-lipoxygenase (5-LO) signaling pathway and its effect on liver injury in Aluminum-Overloaded rats. A rat hepatic injury model of chronic Aluminum injury was established via the intragastric administration of Aluminum gluconate (Al(3+) 200mg/kg per day, 5days a week for 20weeks). The 5-LO inhibitor, caffeic acid (10 and 30mg/kg), was intragastrically administered 1h after Aluminum administration. Hematoxylin and eosin staining was used to visualize pathological changes in rat liver tissue. A series of biochemical indicators were measured with biochemistry assay or ELISAs. Immunochemistry and RT-PCR methods were used to detect 5-LO protein and mRNA expression in the liver, respectively. Caffeic acid administration protected livers against histopathological injury, decreased plasma ALT, AST, and ALP levels, decreased TNF-α, IL-6, IL-1β and LTs levels, increased the reactive oxygen species content, and down-regulated the mRNA and protein expressions of 5-LO in Aluminum Overloaded rats. Our results indicate that 5-lipoxygenase activation is mechanistically involved in chronic hepatic injury in a rat model of chronic Aluminum Overload exposure and that the 5-LO signaling pathway, which associated with inflammation and oxidative stress, is a potential therapeutic target for chronic non-infection liver diseases.

Hui Xia - One of the best experts on this subject based on the ideXlab platform.

  • treatment with either cox 2 inhibitor or 5 lox inhibitor causes no compensation between cox 2 pathway and 5 lox pathway in chronic Aluminum Overload induced liver injury in rats
    Fundamental & Clinical Pharmacology, 2019
    Co-Authors: Hui Xia, Hong Wang, Yongming Wang, Yang Yang, Jiahua Zhang, Zhihao Chen, Junqing Yang
    Abstract:

    This study was designed to observe the compensation between cyclooxygenase-2 pathway and 5-lipoxygenase pathway in chronic Aluminum Overload-induced liver injury rats. A rat hepatic injury model of chronic Aluminum injury was established by the intragastric administration of Aluminum gluconate (Al3 + 200 mg/kg per day, 5 days a week for 20 weeks). The COX-2 inhibitor [meloxicam (1 mg/kg)] and 5-LOX inhibitor [caffeic acid (30 mg/kg)] were intragastrically administered 1 h after Aluminum administration. The histopathology was detected by hematoxylin-eosin staining. A series of biochemical indicators were measured with biochemistry assay or ELISAs. The expressions of COX-2 and 5-LOX were measured by immunohistochemistry. Our experimental results showed that Aluminum Overload caused a significant damage to the liver and also significantly increased the expressions of COX-2, 5-LOX and the levels of inflammation and oxidative stress. The administration of meloxicam and caffeic acid significantly protected livers against histopathological injury, significantly decreased plasma ALT, AST, and ALP levels, significantly decreased TNF-α, IL-6, IL-1β levels, and oxidative stress. However, the administration of caffeic acid did not significantly increase the expression of COX-2 compared with the model group. On the other hand, the administration of meloxicam also did not significantly increase the expression of 5-LOX compared with the model group. Our results indicate that there is no compensation between COX-2 pathway and 5-LOX pathway by inhibiting either COX-2 or 5-LOX in chronic Aluminum Overload-induced liver injury rat.

  • cysltr1 blockage ameliorates liver injury caused by Aluminum Overload via pi3k akt mtor mediated autophagy activation in vivo and in vitro
    Molecular Pharmaceutics, 2018
    Co-Authors: Junqing Yang, Hui Xia, Yang Yang, Jiahua Zhang, Zhihao Chen, Ying Luo, Lu Yang, Dongzhi Ran, Hong Wang
    Abstract:

    Aluminum (Al) is a trivalent cation that can accumulate in animal organs, especially in the liver. We previously demonstrated that Al-Overload could induce liver morphologic aberrations and dysfunction. However, the molecular mechanism underlying liver injury caused by Al-Overload still remains unknown. In the present study, we investigated the relationship between leukotrienes receptors and the PI3K/AKT/mTOR pathway in Al-induced liver injury in vivo and in vitro. We demonstrated that Al-Overload significantly increased the protein expression levels of CysLTR1, PI3K, AKT, mTOR, and p62, while significantly decreasing the LC3BII protein levels in rat liver; thus, suggesting that the autophagy process was inhibited in Al-Overloaded rat liver. In addition, MK-571, an inhibitor of CysLTR1, effectively protected the human hepatocyte L02 cells against injury caused by Al exposure. Moreover, CysLTR1 blockage could significantly down-regulate the PI3K/AKT/mTOR pathway and activate autophagy. The effect of MK-571...

Yang Jun - One of the best experts on this subject based on the ideXlab platform.

  • effect of cox 2 inhibitor on 5 lo expression of hippocampus in chronic Aluminum Overload induced neurodegenerative rats
    Chinese Journal of Gerontology, 2012
    Co-Authors: Yang Jun
    Abstract:

    Objective To investigate the effect of meloxicam on 5-LO expression of hippocampus in chronic Aluminum Overload induced neurodegeneration rats.Methods Neurodegeneration model of Wistar rats were established by intragastric administration of Aluminum gluconate(Al3+200 mg/kg),once a day,5 d/week,for 20 weeks.Meloxicam(1 and 3 mg/kg) was intragastrically administered 30 min after each Aluminum administration.The expression of 5-LO mRNA and protein in hippocampus were detected by RT-PCR and Western blot respectively.Results Expression of 5-LO mRNA and protein in hippocampus obviously were increased.Meloxicam obviously protected rats from learning and memory function impairment and neuron death,significantly inhibited increase of the expression of 5-LO mRNA and protein induced by chronic Aluminum Overload.Conclusions Meloxicam can downregulate the 5-LO expression of hippocampus in chronic Aluminum Overload induced neurodegenerative rats.

  • experimental study on relationship between 5 lo expression and brain damage induced by chronic Aluminum Overload in rats
    Chinese Journal of Gerontology, 2011
    Co-Authors: Yang Jun
    Abstract:

    Objective To explore the relationship between 5-LO expression and brain damage induced by chronic Aluminum Overload in rats.Methods The brain injury model of rats was established via intragastric administration of Aluminum gluconate(element Aluminum 200 mg/kg) once a day,5 d/w for 20 weeks.The 5-LO inhibitor caffeic acid(30,10 mg/kg) was intragastrically administered 1 h after Aluminum administration.Pathomorphological changes of hippocampal neuron and the spatial learning and memory function were observed.The 5-LO mRNA expression in hippocampus was detected by RT-PCR and the 5-LO protein in hippocampus was detected by Western-blot.Results Chronic Aluminum Overload could markedly induce spatial learning and memory function impairment and hippocampal neuronal injury in rats.The 5-LO mRNA expression and 5-LO protein significantly increased in chronic Aluminum Overload rats.The administration of the caffeic acid could significantly prevent rats from learning and memory function impairments and hippocampus neuronal death.Caffeic acid also obviously decreased 5-LO mRNA expression and 5-LO protein of chronic Aluminum Overload rats.Conclusions There is a close connection between over-expression of 5-LO and neuron damage induced by chronic Aluminum Overload.And administration of selective inhibitor of 5-LO can prevent the rat brain from damage induced by chronic Aluminum Overload.

  • protective effect of meloxicam on chronic Aluminum Overload induced neurodegeneration of rats
    Chinese Journal of Gerontology, 2009
    Co-Authors: Yang Jun
    Abstract:

    Objective To investigate the protective effect of meloxicam on chronic Aluminum Overload-induced neurodegeneration of rats.Methods The neurodegeneration models of Wistar rats were established by intragastric administration of Aluminum gluconate for 20 weeks,and Aluminum gluconate was given once a day and 5 days every week.Meloxicam(1 and 3 mg/kg) was intragastrically administered after Aluminum administration 30 minutes.Spatial learning and memory function of rats were determined by Morris water maze.Morphologic changes of hippocampal neurons were evaluated by HE staining.The activity of acetylcholine esterase(AchE),monoamine oxidase-B(MAO-B) and superoxide dismutase(SOD) and the content of malondialdehyde(MDA) was detected by biochemistry enzymology.Results The spatial learning and memory function of chronic Aluminum Overload rats were significantly impaired.Hippocampal neurons in model rats showed obviously karyopycnosis.The content of MDA and the activity of AchE and MAO-B in hippocampus obviously increased,and the activity of SOD significantly decreased.Meloxicam improved the impairment of learning and memory function and neurons damage in hippocampus,and significantly inhibited the increasing of activities AchE and MAO-B and content of MDA,and the decreasing of activities of SOD of rats with Aluminum Overload.Conclusions Meloxicam has protective effect on neurodegeneration induced by chronic Aluminum Overload in rats.

  • effect of meloxicam on cyclooxygenase 2 expression of chronic Aluminum Overload induced nerve degenaration in rat hippocampus
    Chinese Journal of Pharmacology and Toxicology, 2009
    Co-Authors: Yang Jun
    Abstract:

    AIM To investigate the effect of cyclooxygenase2(COX-2) inhibitors on COX-2 expression of nerve degeneration in rat hippocampus. METHODS The rats were divided into 4 groups: normal control,chronic Aluminum Overload model,and meloxicam 1 and 3 mg·kg-1 groups. Except normal control group,the rats were ig given Aluminum gluconate(Al3+ 200 mg·kg-1·d-1),5 d a week,for 20 weeks. Meloxicam was administered ig to the rats in meloxicam groups 30 min after each Aluminum administration. Spatial learning and memory function of rat was determined with Morris water maze,morphologic changes in hippocampal neurons were evaluated by HE staining,and COX-2 mRNA and protein expressions in hippocampus were detected with RT-PCR and Western blot,respectively. RESULTS Compared with normal control group,the spatial learning and memory function of rats in chronic Aluminum Overload model group was significantly impaired,and hippocampal neurons showed obviously karyopycnosis. The expressions of COX-2 mRNA and protein in hippocampus obviously increased,too. Meloxicam 1 and 3 mg·kg-1 obviously prevented rats from learning and memory function impairment induced by chronic Aluminum Overload,and decreased the percentage of neuron with karyopycnosis. The increase in COX-2 mRNA and protein expressions induced by chronic Aluminum Overload was significantly inhibited by meloxicam. CONCLUSIONMeloxicam can inhibit the COX-2 expression of neurodegeneration induced by chronic Aluminum Overload in rat hippocampus,and it is suggested that the COX-2 inhibitors use to prevent and treat the neurodegenerative diseases.