中文摘要：

目的探讨c-Jun氨基端激酶（JNK）活化及其介导凋亡信号通路在小鼠小肠缺血再灌注损伤中的作用。方法C57 BL/6小鼠随机分为假手术组（S）和缺血再灌注不同时间[即刻（0）、0.5、1、4、6、12 h]组,夹闭肠系膜前动脉40 min后再灌注造成小肠缺血再灌注损伤模型,假手术组不夹闭动脉。假手术后及再灌注后不同时间处死小鼠取小肠标本,Western印迹法检测小肠JNK、磷酸化JNK、Cleaved-caspase-3、Bcl-2和Bax蛋白表达水平,观察回肠组织病理学改变。结果肠缺血再灌注早期肠组织病理损伤最重,至12 h肠组织结构基本恢复正常。肠缺血及再灌注早期,小肠组织JNK持续活化,与假手术组比较差异有统计学意义（P〈0.01）;与假手术组比较,再灌注0.5、1 h小肠组织Cleaved-caspase-3明显增加（P〈0.01）,同时抗凋亡Bcl-2蛋白明显下调（P〈0.01）,各组间促凋亡蛋白Bax表达无统计学差异。结论肠缺血再灌注早期小肠组织JNK活化、抗凋亡蛋白Bcl-2表达下调,可能参与了caspase-3依赖的细胞凋亡和组织损害。

英文摘要：

Objective To explore the role of c-Jun NH2 terminal kinase（JNK） activation and JNK-mediated apoptotic signal pathway in intestinal ischemia/reperfusion（II/R） in mice.Methods C57BL/6 mice were randomly divided into sham-operated group（n=6） and II/R groups（n=36）;the latter was further divided according to time after perfusion（0,0.5,1,4,6 and 12 h）.Animal II/R model was established by clamping the superior mesenteric artery（SMA） for 40 min followed by reperfusion.Animals in the sham-operated group received no clamping.Animals in the two groups were sacrificed at defined time points,and the expression of JNK,phosphorylation（phospho-） JNK,cleaved caspase-3,Bcl-2 and Bax protein in the intestinal tissue was examined by Western blotting analysis,and the pathological changes of ileum tissue were observed under optical microscope.Results Most severe intestinal injury was found at the early stage of reperfusion,and the intestinal tissues almost recovered 12 h later.The phospho-JNK in the intestine was significantly elevated within 1 h after II/R compared with sham group（P〈0.01）.Cleaved caspase-3 was significantly increased in II/R group at 0.5 h,1 h after reperfusion compared to sham group（P〈0.01）;the expression of Bcl-2 protein in II/R group was significantly decreased compared with the sham-operated group（P〈0.01）,and there was no significant difference in Bax expression between different groups.Conclusion JNK phosphorylation plays an essential role in the intestinal damages induced by II/R,possibly through down-regulating Bcl-2 protein expression and caspase-3 dependent apoptosis pathway.