Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family...Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in celt apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1,3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.展开更多
OBJECTIVE The aim of the present study was to evaluate the protective effects of momordica charantia polysaccharides(MCP) on depressive animal model induced by chronic social defeat stress(CSDS) and explore the underl...OBJECTIVE The aim of the present study was to evaluate the protective effects of momordica charantia polysaccharides(MCP) on depressive animal model induced by chronic social defeat stress(CSDS) and explore the underlying mechanisms.METHODS We established CSDS depressant mouse model and treated CSDS mice with MCP.Sucrose preference,forced swim test(FST) and social interaction test(SIT) were used to measure behaviors changes.We used ELISA,Q-PCR and western blot to test the levels of cytokines in the hippocampus.RESULTS The results showed that chronic administration of MCP(100,200 and 400 mg·kg^(-1)) significantly prevented depressive-like behaviors in mice as assessed by social interaction(SIT),tail suspension(TST) and sucrose preference tests(SPT).It was showed that the elevation of proinflammatory cytokines(TNF-α,IL-6,and IL-β) concentra.tions,up-regulation of JNK3,c-Jun,and P-110β protein expressions in the hippocampus of CSDS model.Moreover,reduction activity of PI3K and phosphorylation level of protein kinase B(AKT) was also observed in the hippocampus of CSDS model.All above phenomenon were reversed after MCP intervened.Further.more,the protective effects of MCP on the CSDS mice were partly inhibited by the specific phosphati.dylinositol 3-kinase(PI3K) inhibitor,LY294002.CONCLUSION The protective effects of MCP against depressive-like effects in CSDS mice might reduce neuroinflammatory and involve in attenuation of JNK3/PI3K/AKT pathway in the hippocampus.展开更多
文摘Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in celt apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1,3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.
基金supported by the Yichang Key Laboratory of Ischemic Cardiovascular and Cerebrovascular Disease Translational Medicine Foundation for Generous Financial Support(2017KXN09)
文摘OBJECTIVE The aim of the present study was to evaluate the protective effects of momordica charantia polysaccharides(MCP) on depressive animal model induced by chronic social defeat stress(CSDS) and explore the underlying mechanisms.METHODS We established CSDS depressant mouse model and treated CSDS mice with MCP.Sucrose preference,forced swim test(FST) and social interaction test(SIT) were used to measure behaviors changes.We used ELISA,Q-PCR and western blot to test the levels of cytokines in the hippocampus.RESULTS The results showed that chronic administration of MCP(100,200 and 400 mg·kg^(-1)) significantly prevented depressive-like behaviors in mice as assessed by social interaction(SIT),tail suspension(TST) and sucrose preference tests(SPT).It was showed that the elevation of proinflammatory cytokines(TNF-α,IL-6,and IL-β) concentra.tions,up-regulation of JNK3,c-Jun,and P-110β protein expressions in the hippocampus of CSDS model.Moreover,reduction activity of PI3K and phosphorylation level of protein kinase B(AKT) was also observed in the hippocampus of CSDS model.All above phenomenon were reversed after MCP intervened.Further.more,the protective effects of MCP on the CSDS mice were partly inhibited by the specific phosphati.dylinositol 3-kinase(PI3K) inhibitor,LY294002.CONCLUSION The protective effects of MCP against depressive-like effects in CSDS mice might reduce neuroinflammatory and involve in attenuation of JNK3/PI3K/AKT pathway in the hippocampus.
基金supported by the Beijing Natural Science Foundation(Grant No.2123062)Research Fund for the Doctoral Program of Higher Education of China(Grant No.20121103120008)Science and Tech-nology Foundation of Beijing University of Technology(Grant No.ykj-2012-8725)
