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目的观察兰茵凤扬化浊解毒方对溃疡性结肠炎(UC)大鼠TNF-α、TLR4及NF-kBp65表达的影响,以探讨其作用机制。方法将60只8周龄健康雄性Wistar大鼠随机分为5组,每组12只,分别为正常组、模型组、中药大剂量组、中药小剂量组和SPAP组。采用TNBs/乙醇法诱导溃疡性结肠炎模型,造模成功后分别对中药大剂量组(20.0g/kg)、中药小剂量组(5.0g/kg)及SPAP(0.3g/kg)灌胃给予相应的药物,每次2.5ml;正常组、模型组给予等容量的0.9%NaCl溶液。各组均每日1次,连续14天。观察各组大鼠一般情况以及DAI评分、组织病理学、TNF-α、TLR4、NF-kBp65变化情况。结果与正常组比较,模型组DAI评分、TNF-α、TLR4及NF-kBp65含量均有升高(P<0.05);与模型组比较,中药大、小剂量组各指标均下降(P<0.05);中药大、小剂量组比较,差异均有统计学意义(P<0.05);中药大剂量组与SPAP组比较,差异有统计学意义(P<0.05);中药小剂量组与SPAP组比较,差异均无统计学意义(P>0.05)。结论兰茵凤扬化浊解毒方对UC模型大鼠有较好的治疗作用,其疗效与中药剂量大小有关;其机制可能是通过对TNF-α等促炎因子的调节来调控TLRs/NF-kB通路,抑制NF-kB的活化及释放,起到抗炎和调节免疫作用。
Objective To observe the effect of LanYin Feng Yang Hua Zhuo Jie Du Fang on the expression of TNF-α, TLR4 and NF-κB p65 in rats with ulcerative colitis (UC) to investigate its mechanism. Methods Sixty healthy male Wistar rats of 8 weeks old were randomly divided into 5 groups (n = 12): normal group, model group, high dose group, low dose group and SPAP group. The model of ulcerative colitis was induced by TNBs / ethanol method. After the model was successfully established, the rats were given intragastric administration of high dose group (20.0g / kg), low dose group (5.0g / kg) and SPAP (0.3g / kg) The corresponding drugs, each 2.5ml; normal group, the model group was given 0.9% NaCl solution of equal capacity. Each group was once daily for 14 consecutive days. The general situation and the changes of DAI score, histopathology, TNF-α, TLR4 and NF-κB p65 in each group were observed. Results Compared with the normal group, DAI score, TNF-α, TLR4 and NF-kBp65 contents in the model group were significantly increased (P <0.05). Compared with the model group, (P <0.05). Compared with SPAP group, the difference was statistically significant (P <0.05); Compared with the SPAP group, the traditional Chinese medicine low-dose group , There was no significant difference (P> 0.05). Conclusions LanYin Feng Yang Hua Zhuo Jie Du decoction has a good therapeutic effect on UC model rats, and its curative effect is related to the dose of Chinese medicine. The mechanism may be that the regulation of TLRs / NF- kB pathway, inhibition of NF-kB activation and release, play an anti-inflammatory and immune regulation.