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目的:探讨复方甘草酸苷对溃疡性结肠炎大鼠Toll样受体介导的NF-κB信号通路的影响。方法:健康SD大鼠49只取10只作为正常对照组(A组),其余39只大鼠采用TNBS/乙醇联合建模法制备溃疡性结肠炎大鼠模型,39只大鼠再随机平分为模型对照组(B组),柳氮磺吡啶组(C组)、复方甘草酸苷组(D组),分别给予生理盐水、柳氮磺吡啶与复方甘草酸苷干预处理。结果:肉眼与病理学观察发现大鼠溃疡性结肠炎模型造模成功。复方甘草酸苷组的血清TLR4与NF-κB p65表达量明显低于模型对照组,与柳氮磺吡啶组及正常对照组比较差异无统计学意义(P>0.05)。正常对照组的NF-κB p65与TLR4蛋白阳性表达率明显低于模型对照组,与柳氮磺吡啶组与复方甘草酸苷组对比无明显差异(P>0.05)。Pearson相关分析显示NF-κB p65与TLR4在溃疡性结肠炎模型中的表达呈正相关关系(P<0.05)。结论:Toll样受体介导的核因子-κB信号通路在溃疡性结肠炎的发生发展中起重要作用,复方甘草酸苷可阻断该通路中TLR与NF-κB p65的表达,进而为临床用药提供理论依据。
Objective: To investigate the effects of compound glycyrrhizin on Toll-like receptor-mediated NF-κB signaling in ulcerative colitis rats. Methods: Ninety-four healthy SD rats were selected as the normal control group (group A). The remaining 39 rats were used to establish a rat model of ulcerative colitis by TNBS / ethanol combined modeling. 39 rats were randomly divided into The model control group (group B), sulfasalazine group (group C) and compound glycyrrhizin group (group D) were given physiological saline, sulfasalazine and compound glycyrrhizin for intervention. Results: The model of ulcerative colitis in rats was successfully established by naked eye and pathology. The expression of TLR4 and NF-κB p65 in compound glycyrrhizin group was significantly lower than that in model control group, but no significant difference compared with sulfasalazine group and normal control group (P> 0.05). The positive expression rates of NF-κB p65 and TLR4 in normal control group were significantly lower than those in model control group, but there was no significant difference between sulfasalazine group and compound glycyrrhizin group (P> 0.05). Pearson correlation analysis showed that there was a positive correlation between the expression of NF-κB p65 and TLR4 in ulcerative colitis model (P <0.05). Conclusion: Toll-like receptor-mediated nuclear factor-κB signaling plays an important role in the development of ulcerative colitis. Compound glycyrrhizin can block the expression of TLR and NF-κB p65 in this pathway, Provide a theoretical basis for medication.