2012Zhongguo bingli shengli zazhiRequires access

JNK pathway promotes apoptosis of rat hippocampal neurons after cerebral ischemia and reperfusion

Shasha Liu

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Abstract

AIM:To investigate the effect of c-Jun N-terminal kinase(JNK) pathway on the apoptosis of hippocampal neurons after cerebral ischemia-reperfusion(IR) in SD rats.METHODS: Ninety rats were randomly divided into 5 groups: sham group,cerebral IR group,cerebral IR+JNK inhibitor(SP600125) group,cerebral IR+JNK agonist(anisomycin) group and cerebral IR+vehicle group.The brain samples were collected 24 h after reperfusion.The protein level of caspase-3 in hippocampal neurons was measured by immunohistochemical and Western blotting techniques.The mRNA expression of caspase-3 in the hippocampus was determined by real-time fluorescence quantitative PCR.The apoptosis of hippocampal neurons was detected by TUNEL staining.RESULTS: Compared with sham group,the expression of caspase-3 at mRNA and protein levels in cerebral IR group increased obviously(P0.05).Compared with cerebral IR group,the expression of caspase-3 at mRNA and protein levels in cerebral IR+JNK inhibitor group decreased obviously(P0.05),and those in cerebral group increased obviously(P0.05).However,the expression of caspase-3 at mRNA and protein levels in cerebral IR+vehicle group had no obvious change(P0.05).The apoptosis of hippocampal neurons in each group was consistent with the changes of caspase-3 at mRNA and protein levels.CONCLUSION: Activation of JNK pathway enhances caspase-3 expression in rat hippocampal neurons after cerebral IR,thus promoting the apoptosis of the neurons.

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AIM:To investigate the effect of c-Jun N-terminal kinase(JNK) pathway on the apoptosis of hippocampal neurons after cerebral ischemia-reperfusion(IR) in SD rats.METHODS: Ninety rats were randomly divided into 5 groups: sham group,cerebral IR group,cerebral IR+JNK inhibitor(SP600125) group,cerebral IR+JNK agonist(anisomycin) group and cerebral IR+vehicle group.The brain samples were collected 24 h after reperfusion.The protein level of caspase-3 in hippocampal neurons was measured by immunohistochemical and Western blotting techniques.The mRNA expression of caspase-3 in the hippocampus was determined by real-time fluorescence quantitative PCR.The apoptosis of hippocampal neurons was detected by TUNEL staining.RESULTS: Compared with sham group,the expression of caspase-3 at mRNA and protein levels in cerebral IR group increased obviously(P0.05).Compared with cerebral IR group,the expression of caspase-3 at mRNA and protein levels in cerebral IR+JNK inhibitor group decreased obviously(P0.05),and those in cerebral group increased obviously(P0.05).However,the expression of caspase-3 at mRNA and protein levels in cerebral IR+vehicle group had no obvious change(P0.05).The apoptosis of hippocampal neurons in each group was consistent with the changes of caspase-3 at mRNA and protein levels.CONCLUSION: Activation of JNK pathway enhances caspase-3 expression in rat hippocampal neurons after cerebral IR,thus promoting the apoptosis of the neurons.

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Available abstract

AIM:To investigate the effect of c-Jun N-terminal kinase(JNK) pathway on the apoptosis of hippocampal neurons after cerebral ischemia-reperfusion(IR) in SD rats.METHODS: Ninety rats were randomly divided into 5 groups: sham group,cerebral IR group,cerebral IR+JNK inhibitor(SP600125) group,cerebral IR+JNK agonist(anisomycin) group and cerebral IR+vehicle group.The brain samples were collected 24 h after reperfusion.The protein level of caspase-3 in hippocampal neurons was measured by immunohistochemical and Western blotting techniques.The mRNA expression of caspase-3 in the hippocampus was determined by real-time fluorescence quantitative PCR.The apoptosis of hippocampal neurons was detected by TUNEL staining.RESULTS: Compared with sham group,the expression of caspase-3 at mRNA and protein levels in cerebral IR group increased obviously(P0.05).Compared with cerebral IR group,the expression of caspase-3 at mRNA and protein levels in cerebral IR+JNK inhibitor group decreased obviously(P0.05),and those in cerebral group increased obviously(P0.05).However,the expression of caspase-3 at mRNA and protein levels in cerebral IR+vehicle group had no obvious change(P0.05).The apoptosis of hippocampal neurons in each group was consistent with the changes of caspase-3 at mRNA and protein levels.CONCLUSION: Activation of JNK pathway enhances caspase-3 expression in rat hippocampal neurons after cerebral IR,thus promoting the apoptosis of the neurons.

Key concepts: Hippocampal formation, TUNEL assay, Anisomycin, Apoptosis, Messenger RNA, Hippocampus, Caspase 3, Internal medicine

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