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目的:观察化浊解毒消痈方对溃疡性结肠炎大鼠Th1/Th2平衡的影响,以探讨其作用机制。方法:将Wistar大鼠随机分为正常组、模型组、阳性对照柳氮磺胺吡啶组、化浊解毒消痈全方组、化浊方组、解毒方组、每组10只。以三硝基苯磺酸/乙醇法建立溃疡性结肠炎大鼠动物模型,造模成功后分别予化浊解毒消痈方31.8g/kg、化浊方19.3g/kg、解毒方19.3g/kg灌胃,SASP组予柳氮磺胺吡啶(0.5 g/kg)灌胃,模型组及正常组每日以蒸馏水10ml/kg灌胃,均连续14d。观察各组大鼠一般情况及疾病活动指数(DAI)评分、组织病理学、SOD含量、血清及结肠组织IFN-γ、IL-4、IFN-γ/IL-4变化情况。结果:化浊解毒消痈全方(31.8g/kg)、化浊方(19.3g/kg)、解毒方(19.3g/kg)和柳氮磺胺吡啶肠溶片(0.5g/kg)可改善大鼠的一般情况,降低DAI评分,提高SOD含量,同时能降低血液及结肠组织中IFN-γ水平,提高IL-4水平,降低IFN-γ/IL-4比值,其中以化浊解毒消痈全方组(31.8g/kg)作用效果更为显著。结论 :化浊解毒消痈方药能显著改善造模大鼠症状,通过下调Th1细胞因子分泌和上调Th2细胞因子水平,恢复Th1/Th2平衡,发挥抗炎治疗作用。
Objective: To observe the effect of Huazhuo Jiedu Xiaoyu Recipe on Th1 / Th2 balance in rats with ulcerative colitis, and to explore its mechanism. Methods: Wistar rats were randomly divided into normal group, model group, positive control sulfasalazine group, Huazhuo Jiedu Decoction total group, Huazhuo prescription group and Jiedu prescription group, 10 in each group. The rat model of ulcerative colitis was established by trinitrobenzene sulfonic acid / ethanol method. After the model was established, the rats were treated with Huazhuo Jiedu Decoction 31.8g / kg, Huazhuo 19.3g / kg, detoxification 19.3g / kg, SASP group was given sulfasalazine (0.5 g / kg) by intragastric administration. The model group and the normal group were intragastrically administered with distilled water 10 ml / kg for 14 days. The changes of DAI score, histopathology, SOD content, IFN-γ, IL-4 and IFN-γ / IL-4 in serum and colon tissues of rats in each group were observed. Results: Huazhuo Jiedu Decoction (31.8g / kg), Huazhuo Fang (19.3g / kg), detoxification side (19.3g / kg) and sulfasalazine enteric-coated tablets (0.5g / kg) The general situation of rats, reduce the DAI score, increase the content of SOD, while reducing blood and colon tissue IFN-γ levels, raise the level of IL-4 and reduce the ratio of IFN-γ / IL-4, The whole group (31.8g / kg) effect is more pronounced. Conclusion: Huazhuo Jiedu Decoction can significantly ameliorate the symptoms of model rats. It can restore the Th1 / Th2 balance by down-regulating the secretion of Th1 cytokines and up-regulating the level of Th2 cytokines and exert anti-inflammatory therapeutic effect.