[Protective effects and mechanism of SP600125 on lung ischemia/reperfusion injury in rats].

Objective: To investigate the protective effects and mechanism of SP600125-specificity inhibitor of c-Jun N-terminal kinase(JNK)on lung ischemia /reperfusion injury in rats.Methods: The unilateral lung ischemia/reperfusion model was replicated in vivo.Rats were randomly divided into three groups(n=10): control group,ischemia/reperfusion group(I/R group) and ischemia/reperfusion + SP600125 group(SP600125 group).The lung tissues sampled at the end of each experiment were assayed for wet/dry weight ratio(W/D),the injured alveoli rate(IAR),the expression of phosphorylation JNK(p-JNK) and JNK protein were detected by Western blot,the expression of Bcl-2,Bax,Caspase3 protein were detected by immunocytochemistry techniques,the pneumocyte apoptosis index(AI) was detected by terminal deoxynucleotidy1 transferase mediated dUTP nick end abeling(TUNEL),the ultrastructure changes were observed under electron microscope.Results: Compared to I/R group,the expression of p-JNK,Bcl-2,Bax and caspase-3 protein were markedly decreased(all P0.01),the expression of Bcl-2 protein and the ratio of Bcl-2/Bax were markedly increased in SP600125 group(all P0.01).The value of AI,W/D,IAR showed significantly lower than those in I/R group(all P0.01).Meanwhile,light morphological and ultrastructure injury were found in SP600125 group.Conclusion: SP600125 can suppress JNK signal pathway,up-regulate the ratio of Bcl-2/Bax to inhibit Caspase-3 dependent apoptosis,so that it protects lung tissue from ischemia/reperfusion injury.