Objective:To analysis the pathological structure of colon wall and the change of myenteric plexus' vasoactive in-testinal peptidergic(VIP) neurons expression, and to explore the pathological mechanism of neurogenic bowel dys-function(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, ede-ma, erosion,villi reducingjodging and falling-off were observed,and the colon tissue's VIPmRNA and protein ex-pression 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.%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N YU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Western blot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.
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