清化肠饮治疗溃疡性结肠炎大鼠模型的实验性研究

目的]探索清化肠饮对溃疡性结肠炎（UC）大鼠的治疗作用及其机制.方法]将60只健康SPF级Wistar大鼠（雌雄各半）,随机分成正常组,模型对照组,清化肠饮高、中、低剂量组和美沙拉秦组.除正常组外,其余各组均采用免疫复合法造模.观察大鼠疾病活动指数（DAI）,ELISA法测定各组大鼠血清TNF-α、IL-6、IL-8及IL-10的变化情况.结果]治疗前,正常组DAI与各造模组差异均有统计学意义（P＜0.01）;给药2周后,与模型对照组比较,清化肠饮高剂量组、美沙拉秦组大鼠显著降低（P＜0.01）.从大鼠血清上看,与正常组比较,模型对照组大鼠TNF-α、IL-6及IL-8显著增高（P＜0.01）,而IL-10则显著降低（P＜0.01）;与模型对照组比较,清化肠饮高剂量组、美沙拉秦组大鼠TNF-α、IL-6及IL-8显著降低（P＜0.01）,IL-10则显著增高（P＜0.01）;与美沙拉秦组比较,清化肠饮中、低剂量组大鼠TNF-α、IL-6及IL-8显著增高（P＜0.01）,而IL-10则显著降低（P＜0.01）.结论]高剂量清化肠饮是治疗UC的有效药物,通过调节炎性细胞因子的平衡可能是其作用机制之一.

Research of Qinghuachang Yin for the treatment of ulcerative colitis in rats

Objective]To explore the effects and mechanisms of Qinghuachang Yin （QY） in rats with ulcerative colitis（UC）. Methods]Sixty SPF healthy Wistar rats,half male and half female,were randomly divided into normal group, model control group, QY groups with high, moderate and low dosages, mesala- zine group. Rat models were established by immune complex method. Disease activity index（DAD was ob served. Serum levels of TNF-α,IL-6,1L-8 and IL-10 were detected by ELISA. Results]Before the treat- ment,DAI of the model groups were significantly higher than the normal group（P〈0.01）. After two weeks of treatment, compared to that of model control group,DIA of QY group with high dosage and me salazine group decreased significantly（P〈0.01）. Compared to that of normal group, the levels of TNF-α, IL-6 and IL-8 levels of model control group increased significantly（P〈0.01）,while IL-10 level decreased significantly （P〈0.01）. Compared to model control group, the TNF-α, IL-6 and IL-8 levels of QY group with high dosage and mesalazine group decreased significantly（P〈0.01）, while the IL-10 level increased significantly（P〈0.01）. Compared to mesalazine group, TNF-α,IL-6 and IL-8 levels of QY groups with moderate and low dosages increased significantly（P〈0.01）,while the IL-10 level decreased significantly（P〈0. 01）. I-Conclusion]High-dose of QY is an effective drug for UC treatment. Regulating the balance of in- flammatory cytokines may be one of the potential mechanism for the treatment of UC .