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目的:研究姜黄素治疗溃疡性结肠炎的作用及其机制。方法:用2,4二硝基氯苯(DNCB)建立大鼠创伤性溃疡结肠炎模型,观察姜黄素对其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)和结肠黏膜过氧化脂质(LPO)的影响。结果:造模大鼠经姜黄素治疗,结肠黏膜光镜下组织学有显著改变,结肠损伤分数、大便乳酸含量降低,红细胞SOD活性升高,肠黏膜LPO含量降低,TLR4、TLR2因子表达进一步减弱,疗效优于阳性对照组(P<0.01)。结论:姜黄素发挥抗溃疡性结肠炎的机制之一可能与其减弱TLR4、TLR2的表达,降低结肠黏膜LPO含量,增加红细胞SOD活性,进而增加机体对O2.-的清除,从而促进大便乳酸排泄,减少结肠炎症损伤有关。
Objective: To study the effect of curcumin on ulcerative colitis and its mechanism. Methods: The rat model of traumatic ulcer colitis was established by using 2,4-dinitrochlorobenzene (DNCB). The effects of curcumin on the histopathology, colonic damage, erythrocyte superoxide dismutase (SOD) and colon Effects of mucosal lipid peroxides (LPO). Results: After treated by curcumin, the histology of colonic mucosa of colon mucosa was significantly changed. Colon injury score, lactic acid content decreased, SOD activity in erythrocytes increased, LPO content in intestinal mucosa decreased and TLR4 and TLR2 expression decreased , The curative effect is better than the positive control group (P <0.01). Conclusion: One of the mechanisms of curcumin in the development of anti-ulcerative colitis may be related to the decrease of TLR4 and TLR2 expression, decrease of LPO content in colonic mucosa, increase of SOD activity of erythrocytes, and then increase of clearance of O2.- to promote lactic acid excretion, Reduce colonic inflammatory damage.