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目的 探讨乌司他丁对溃疡性结肠炎 (UC)的治疗效果及其作用机制。方法 40只成年Wistar鼠 ,随机分为四组 ,正常组 (A组 )、溃疡性结肠炎组 (B组 )、柳氮磺胺吡啶 (SASP)治疗组 (C组 )、乌司他丁治疗组 (D组 ) ,用三硝基苯磺酸 (TNBS)诱导实验性UC的大鼠模型 ,A、B二组用生理盐水处理大鼠。用药治疗 2周后 ,分别观察各组血清中的肿瘤坏死因子α(TNF -α)、丙二醛(MDA)、超氧化物歧化酶 (SOD)的变化以及病理学的改变。结果 乌司他丁、SASP可使实验性UC大鼠血清中的肿瘤坏死因子α、MDA、含量明显下降 ,SOD活性上升 ,并可明显减轻其结肠急性损伤程度及病理学的改变 ,且乌司他丁组疗效优于SASP组。结论 乌司他丁对UC有明显的治疗作用 ,其可能的机制为抑制炎性细胞因子的释放 ,清除自由基。
Objective To investigate the therapeutic effect of ulinastatin on ulcerative colitis (UC) and its mechanism. Methods Forty adult Wistar rats were randomly divided into four groups: normal group (group A), ulcerative colitis group (group B), sulfasalazine group (group C), ulinastatin group (Group D). Rats in experimental UC were induced by trinitrobenzene sulfonic acid (TNBS). Rats in groups A and B were treated with saline. After treatment for 2 weeks, the change of tumor necrosis factor alpha (TNF-alpha), malondialdehyde (MDA), superoxide dismutase (SOD) and pathological changes were observed in each group. Results Ulinastatin and SASP significantly decreased the levels of tumor necrosis factor α and MDA in serum of experimental UC rats and increased the activity of SOD, and significantly reduced the degree of acute colonic injury and pathological changes. Histidine group better than SASP group. Conclusion Ulinastatin has a significant therapeutic effect on UC. Its possible mechanism is to inhibit the release of inflammatory cytokines and to eliminate free radicals.