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目的:观察5-氨基水杨酸(5-ASA)对大鼠实验性结肠炎一氧化氮(NO)、一氧化氮合酶(NOS)水平的影响。方法:55只雄性wistar大鼠随机分为4组,正常对照组(I组)10只,模型组(Ⅱ组),5-ASA灌肠治疗组(Ⅲ组)及生理盐水灌肠组(Ⅳ组)各15只;Ⅱ、Ⅲ、Ⅳ组采用2,4-二硝基氯苯(2,4-dinitrochlorobenzene,DNCB)诱发大鼠实验性结肠炎模型,检测各组肠粘膜匀浆或上清液中NO水平、NOS活性,观察各组的病理学变化。结果:Ⅱ组与Ⅰ组比较,结肠粘膜NOS的活性、NO的水平明显升高。Ⅲ组和Ⅳ组相比NO水平、NOS活性明显降低。I组未见明显病理学变化;Ⅱ组粘膜及粘膜下层明显充血、水肿,炎性细胞浸润,糜烂及溃疡形成;Ⅲ组治疗后溃疡有不同程度修复性改变,而Ⅳ组未见相应改变。结论:5-ASA可抑制NOS活性,减少NO产生,从而减轻结肠粘膜组织损伤。
Objective: To observe the effect of 5-aminosalicylic acid (5-ASA) on the levels of nitric oxide (NO) and nitric oxide synthase (NOS) in rat experimental colitis. Methods: Fifty-five male wistar rats were randomly divided into 4 groups: normal control group (group I), model group (group Ⅱ), 5-ASA enema treatment group (group Ⅲ) and saline group (group Ⅳ) The rats in group Ⅱ, Ⅲ and Ⅳ were induced by 2,4-dinitrochlorobenzene (DNCB) into experimental colitis model, and the intestinal mucosa homogenates or supernatants NO level, NOS activity, observe the pathological changes in each group. Results: Compared with group Ⅰ, the activity of NOS and the level of NO in colonic mucosa were significantly increased in group Ⅱ. In group Ⅲ and group Ⅳ, NOS activity was significantly lower than that in group Ⅳ. There was no obvious pathological change in group I; the mucosa and submucosa of group Ⅱ were obviously hyperemia, edema, inflammatory cell infiltration, erosion and ulceration; the ulcer in group Ⅲ had some degree of repair after treatment, but no change in group Ⅳ. Conclusion: 5-ASA can inhibit NOS activity and reduce NO production, thereby reducing colonic mucosal injury.