APOPTOSIS IN HIPPOCAMPUS AFTER FOCAL CEREBRAL ISCHEMIA REPERFUSION THROUGH JNK SIGNALING PATHWAY IN RATS MODELS

[Objective] To investigate the expression and mechanism of c-Jun N-terminal protein kinase (JNK) pro- tein-dependent activation of caspase signaling pathway in the nerve cell’ s apoptosis in hippocampus in rats after focal cerebral ischemia reperfusion (I / R). [Methods] Replicated the MCAO model of rats. The tissues of hippocampus of rats were sampled, the expression of JNK and caspase-3 protein were determined by Western blotting. The apoptosis of pyramidal neurons was de- tected by TUNEL method. [Results] As comparing with the sham group, the p-c-jun level in the I / R group was significantly enhanced; difference was significant between 3 h, 6 h, 12 h (P﹤0.05). Caspase-3 appeared at 6h after reperfusion (P﹤ 0.05), and it’s peaked at 12 h (P﹤0.05). The quantification of p-c-Jun expression in hippocampus was positively correlated with the expressions of caspase-3 (r = 0.696, P﹤0.01), and the expression of p-c-Jun was positively correlated with the ex- pressions of TUNEL positive cells after I / R (r = 0.310, P﹤0.01). [Conclusion] JNK-dependent activation of caspase signal- ing pathway partly activates the signal transudation of the apoptosis after I / R.