脊髓损伤后大鼠结肠血管活性肠肽能神经元表达的变化

目的:分析大鼠脊髓损伤(SCI)后结肠壁病理结构及结肠肌间神经丛内血管活性肠肽能(VIP)神经元表达变化,探讨脊髓损伤所致神经源性肠道功能障碍(NBD)的病理机制。方法:实验动物分为假手术组、非NBD(对照组)和NBD(模型组);大鼠氯胺酮(60mg/kg)腹腔注射麻醉,利用NYU脊髓打击器,以75gcm致伤力制作第10胸椎节段(T10)SCI模型,手术切除大鼠结肠组织制作标本,采用HE染色法观察结肠壁病理结构,实时逆转录聚合酶链反应(RT-PCR)和Westernblot法检测VIP在mRNA和蛋白水平的表达变化。结果:大鼠SCI后结肠黏膜充血、水肿、糜烂,绒毛减少、倒伏、脱落,结肠组织中VIP的mRNA及蛋白表达水平显著下调,与假手术组、对照组相比差异具有显著性(P<0.05)。结论:结肠VIP能神经元表达变化可能是导致大鼠SCI后NBD的病理机制之一。

Study on the change of vasoactive intestinal peptidergic neurons expression in rat's colon following spinal cord injury

Objective:To analysis the pathological structure of colon wall and the change of myenteric plexus’ vasoactive intestinal peptidergic(VIP)neurons expression,and to explore the pathological mechanism of neurogenic bowel dysfunction(NBD)after spinal cord injury(SCI)in rats.Method:Experimental rats were divided into sham group,non-NBD control group and NBD model group.Weight-drop SCI model was made at T10 segment of rat with N YU impactor device.Colon tissues of rats were resected and the tissue’s pathological structure change by HE dyeing were observed.Colon tissue was examined by real-time RT-PCR and Western blot to analyze the expression of VIP.Result:In model group,the colon intestinal transmission function decreased,and the colonic mucosal hyperemia,edema,erosion,villi reducing,lodging and falling-off were observed,and the colon tissue’s VIPmRNA and protein expression level declined significantly.Compared with sham group and control group,there was significant difference(P<0.05).Conclusion:SCI may result in the change of myenteric plexus’ VIP neurons expression.It is probably one of the pathological mechanisms of NBD after SCI in rats.