脊髓损伤后大鼠结肠血管活性肠肽能神经元表达的变化

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

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。

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 reducing,lodging 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. Author＇s address Department of General Surgery, Beijing Boai Hospital, Capital Medical University School of Rehabilitation Medicine, Beijing, 100068