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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。
Objective To investigate the role of c-Jun N-terminal kinase (JNK) activation and its signal transduction pathways in intestinal ischemia-reperfusion injury in mice. Methods C57 BL / 6 mice were randomly divided into sham operation group (S) and ischemia / reperfusion group (immediate (0), 0.5, 1, 4, 6, 12 h] Reperfusion induced intestinal ischemia-reperfusion injury model, sham-operated group did not clip the artery. Small intestine specimens of mice were killed after sham operation and at different time after reperfusion. The expression of JNK, phosphorylated JNK, Cleaved-caspase-3, Bcl-2 and Bax protein in small intestine was detected by Western blotting. Pathological changes of ileum were observed. Results The pathological changes of intestinal tissue in the early stage of gut ischemia-reperfusion were the heaviest. The intestinal tissue structure returned to normal after 12 hours. Intestinal ischemia and reperfusion early, small intestine JNK continued activation, compared with the sham operation group was statistically significant (P <0.01); compared with the sham operation group, 0.5,1 h reperfusion intestinal tissue Cleaved-caspase-3 significantly (P <0.01). At the same time, anti-apoptotic Bcl-2 protein was significantly down-regulated (P <0.01). There was no significant difference in the expression of pro-apoptotic protein Bax between groups. Conclusion The activation of JNK and the down-regulation of Bcl-2 protein in intestinal tissue may play an important role in caspase-3-dependent apoptosis and tissue damage.