论文部分内容阅读
[目的]研究苦豆子总碱(TASA)治疗溃疡性结肠炎的作用机制。[方法]选取雄性Wistar大鼠96只,随机分为正常对照组、模型组、TASA组和柳氮磺胺吡啶组,每组24只,除正常对照组外,其余3组用2,4二硝基氯苯建立大鼠创伤性溃疡性结肠炎模型,比较4组大鼠结肠黏膜组织病理学、结肠损伤分数、红细胞超氧化物歧化酶(SOD)活性、结肠黏膜过氧化脂质(LPO)含量及肠黏膜周边组织核因子(NF)-κB和白细胞介素(IL)-1β因子的表达。[结果]TASA组大鼠经治疗后,结肠黏膜光镜下组织学有明显改变,结肠损伤分数、大便乳酸含量降低,SOD活性升高,LPO含量降低,NF-κB和IL-1β因子表达进一步下调,与模型组比较差异有统计学意义(P<0.01)。[结论]TASA发挥抗溃疡性结肠炎的机制之一可能与其下调NF-κB和IL-1β的表达,降低结肠黏膜LPO含量,增强红细胞SOD活性,进而增加机体对氧自由基的清除,从而达到促进大便乳酸排泄,减少结肠炎症损伤有关。
[Objective] To study the mechanism of TASA in the treatment of ulcerative colitis. [Methods] Ninety-six male Wistar rats were randomly divided into normal control group, model group, TASA group and sulfasalazine group, with 24 rats in each group. Except normal control group, The rat model of traumatic ulcerative colitis was established by base chlorobenzene. The histopathology, colonic mucosal injury, the activity of erythrocyte superoxide dismutase (SOD) and the content of LPO in colonic mucosa were compared between the four groups. And the expression of nuclear factor (NF) -κB and interleukin (IL) -1β in the surrounding tissues of intestinal mucosa. [Results] The histological changes of colonic mucosa under light microscope in TASA group were significantly changed. The scores of colonic damage, lactic acid content, SOD activity, LPO content, and the expression of NF-κB and IL-1β The difference was statistically significant compared with the model group (P <0.01). [Conclusion] TASA may play an important role in anti-ulcerative colitis by down-regulating the expression of NF-κB and IL-1β, decreasing the content of LPO in colonic mucosa, enhancing the SOD activity of erythrocytes, and then increasing the body’s clearance of oxygen free radicals so as to achieve Promote stool lactic acid excretion, reduce colonic inflammation damage related.