肠道缺血再灌注后GLP-2对黏膜增殖的影响

目的观察胰高血糖素样肽-2(GLP-2)对小鼠肠道缺血再灌注后肠黏膜增殖的影响及机制。方法将30只ICR雄性小鼠随机分为空白对照组、实验对照组和治疗组。实验对照组和治疗组小鼠均制成肠道缺血再灌注模型。实验对照组予PBS液皮下注射,治疗组予GLP-2皮下注射。于术后第5d处死,行不同肠段黏膜形态学检测、细胞增殖核心抗原(PCNA)测定及原位末端标记(INST)染色。结果治疗组各肠段黏膜形态学指标均显著高于实验对照组和空白对照组(均P<0.05),尤以末端回肠为著(P<0.01);治疗组PCNA指数显著高于实验对照组(P<0.01);治疗组细胞凋亡显著低于实验对照组(P<0.01)。结论GLP-2能刺激小肠黏膜上皮增生,抑制凋亡,显著促进肠道缺血再灌注后的黏膜增殖修复。

Effects of GLP-2 on mouse intestinal mucosal proliferation after ischemia/reperfusion insult

Objective To investigate the effects and the underlying mechanism of the glucagons-like peptide 2 (GLP-2) on the intestinal mucosal proliferation after ischemia /reperfusion insult in a mouse model. Methods Thirty ICR male mice were randomly divided into three groups: normal control (N),control (C) and GLP-2 treatment (T). Ischemic injury was induced by ligating the superior mesenteric artery in group C and group T. Mice in group T were injected subcutaneously with GLP-2,while mice in group C were injected subcutaneously with PBS. On the 5th postoperative day,the morphological changes of jejunum and ileum were examined,the expression of proliferating cell nuclear antigen (PCNA) and the cell apoptosis (INST) were assayed. Results The villous height,crypt depth and mucosal thickness of the ileum in group T were significantly higher than those in group C and group N (P<0.05). The crypt PCNA positive index in group T was significantly higher than that of group C (P<0.05). The enterocyte apoptosis in group T was significantly lower than that in group C (P<0.01). Conclusion GLP-2 could enhance small bowel morphological proliferation by stimulating the enterocyte proliferation and decreasing the enterocyte apoptosis in a mouse model of ischemia /reperfusion insult.