[Effect of curcumine on the nuclear pathway of JNK during hippocampal ischemia/reperfusion injury in SHR].

Objective:To investigate the diversify of the nuclear pathway of c-Jun NH2-terminal kinases(JNK) during transient brain ischemia/reperfusion injury in hippocampal neuron apoptosis in spontaneously hypertensive rats(SHR) and to test whether the neuroprotection of curcumine on transient brain ischemia/reperfusion injury in SHR is related to the nuclear pathway of JNK. Methods: Male Wistar-Kyoto(WKY)rats and SHR were randomly divided into five groups(n=6): WKY sham group(W-Sham),WKY ischemia/reperfusion group(W-I/R),SHR sham group(S-Sham),SHR ischemia/reperfusion group(S-I/R) and SHR curcumine (a chinese traditional medicine)100 mg/kg treatment group(S-Cur),which were sacrificed at 2 h,6 h,24 h,3 d and 7 d after reperfusion. Global brain ischemic model was established by 4-VO method.The TdT-mediated dUTP nick end labeling(TUNEL) method was used to detect the neuron apoptosis in hippocampal CA1 region.The immunohistochemical method was applied to investigate the expressions of c-jun and c-fos in hippocampal CA1 region. Results: The expressions of apoptosis and c-jun and c-fos in CA1 region in S-Sham group,W-I/R group and S-I/R group were more than those in W-Sham group(P0.05),were significantly increased in S-I/R group than those in W-I/R group(P0.05),and were significantly decreased in S-Cur group than those in S-I/R group(P0.05). Conclusion: Neuronal apoptosis and the expressions of c-jun and c-fos are more in SHR hippocampal. Global brain ischemia /reperfusion injury induces more expressions of apoptosis in hippocampal neuron in SHR,and the more expressions of c-jun and c-fos may participate in that process. The neuroprotection of curcumine in SHR is related to c-jun and c-fos.