JNK pathway promotes apoptosis of rat hippocampal neurons after cerebral ischemia and reperfusion
Shasha Liu
Abstract
Shasha Liu
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.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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