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目的探讨复方蜥蜴散不同微粒组合剂(下文简称:蜥蜴散)干预大鼠溃疡性结肠炎模型NF-κB信号通路中p65蛋白表达、血清IL-6水平的影响及其治疗UC的可能作用机制。方法将84只雄性SD大鼠随机分为6组:正常对照组(A)、模型组(B)、柳氮磺吡啶肠溶片治疗组(C)、蜥蜴散80目治疗组(D)、蜥蜴散100目治疗组(E)、蜥蜴散80+100目等量混合治疗组(F)。B组及C-F组大鼠采用三硝基苯磺酸(TNBS)乙醇法复制UC模型,A组予生理盐水灌肠处理。造模成功后,实验大鼠灌胃给药,连续给药14d,频次相同,15d后麻醉全部大鼠,行腹主动脉采血取血,取血后取结肠组织病变处包埋。用HE染色观察大鼠结肠黏膜病理改变。用免疫组化法检测肠组织P65蛋白表达。用酶联免疫吸附试验(ELISA法)检测血清白介素6(IL-6)水平。结果蜥蜴散和柳氮磺吡啶肠溶片均可改善UC模型大鼠的一般状况,阻断NF-κB信号通路中p65蛋白表达,降低IL-6水平,其中蜥蜴散80+100目等量混合治疗组作用效果更为明显。结论复方蜥蜴散不同微粒组合剂能减轻UC血清中促炎因子IL-6含量,阻断NF-κB信号通路p65蛋白表达可能对于UC治疗具有重要治疗价值。
Objective To investigate the effect of compound lizards (Lizixisan) on the expression of p65 protein and serum IL-6 in the NF-κB signaling pathway in the rat ulcerative colitis model and its possible mechanism. Methods 84 male SD rats were randomly divided into 6 groups: normal control group (A), model group (B), sulfasalazine enteric-coated treatment group (C), lizards scattered 80 mesh treatment group (D) Lizards scattered 100 mesh treatment group (E), lizards scattered 80 +100 mesh equal mixture treatment group (F). Rats in groups B and C-F were treated with trinitrobenzene sulfonic acid (TNBS) ethanol for UC model. Rats in group A were treated with saline. After successful modeling, the experimental rats were intragastrically administrated for 14 days continuously with the same frequency. After 15 days, all the rats were anesthetized and blood was taken from the abdominal aorta. The blood was removed and the colon tissues were harvested for embedding. The pathological changes of colonic mucosa were observed by HE staining. The expression of P65 protein in intestinal tissue was detected by immunohistochemistry. Serum interleukin 6 (IL-6) levels were measured by enzyme-linked immunosorbent assay (ELISA). Results Both lizards and sulfasalazine enteric-coated tablets could improve the general condition of UC rats, block the expression of p65 protein in NF-κB signaling pathway and decrease the level of IL-6. The effect of treatment group is more obvious. Conclusions The compound lizard powder with different microparticles can reduce the level of proinflammatory cytokine IL-6 in UC serum and block the expression of p65 protein in NF-κB signaling pathway, which may be of great therapeutic value for the treatment of UC.