应激对大鼠结肠神经系统nNOS表达的影响

目的:探讨应激对大鼠结肠神经系统nNOS表达的影响. 方法:SD大鼠30只随机分为对照组,应激组和L-NAME 组,采用水浸-束缚应激(WRS)动物模型,用免疫组织化学ABC法检测nNOS在大鼠结肠黏膜下神经丛和肌间神经丛的表达,应用计算机图像分析系统对其表达进行定量分析．结果:与对照组比较,应激组黏膜下神经丛和肌间神经丛的nNOS阳性神经元的灰度值明显减少(P=0．02或P =0．005),阳性神经元细胞数的平均密度增加(P=0．04 或P=0．01),表达增强,且在黏膜上皮细胞、固有层淋巴细胞也有nNOS表达．L-NAME组黏膜下神经丛和肌间神经丛的nNOS阳性神经元的灰度值较应激组增加 (P=0．04),平均密度下降(P=0．04或P=0．03),表达减弱,而与对照组比较均无明显差异(P>0．05)．结论:应激可引起大鼠结肠神经系统nNOS表达增强, 提示一氧化氮(NO)在应激所致的结肠功能失调中可能起重要作用．

Effect of stress on expression of neuronal nitric oxide synthase in colonic nervous system in rats

AIM: To investigate the effect of stress on the expression of neuronal nitric oxide synthase (nNOS) in colonic nervous system in rats. METHODS: Thirty male SD rats were randomly divided into control group, stress group and NG-nitro-L-arginine methyl ester (L-NAME) group. The rat model of water immersion-restraint stress (WRS) was established. The expression of nNOS in colonic submucous plexus and myenteric plexus in the rats was examined by immuno-histochemical staining and analyzed by computer image analysis system. RESULTS: nNOS immune-positive substance was mostly expressed in the neurons of submucous plexus and myenteric plexus. In comparison with that in control group, the gray value of nNOS positive neurons in submucous plexus and myenteric plexus was significantly decreased (P = 0.02 or P = 0.005), and the density of nNOS positive neurons was increased markedly (P = 0.04 or P = 0.01) in stress group. Moreover, nNOS expression in mucosal epithelial cells and lamina propria lymphocytes were also observed. In comparison with that in stress group, the gray value of nNOS positive neurons in submucous plexus and myenteric plexus was increased (P = 0.04), and the density of nNOS positive neurons was decreased (P = 0.04 or P = 0.03) in L-NAME group. nNOS expression was not significantly different between the rats of L-NAME and control group (P >0.05). CONCLUSION: WRS can increase the expression of nNOS in colonic nervous system in rats, which suggests nitric oxide (NO) may play an important role in WRS-induced function disorder of colon.