论文部分内容阅读
目的:观察表没食子儿茶素没食子酸酯(EGCG)对大鼠TNBS结肠炎的治疗作用,并探讨其可能的抗炎机制。方法:用TNBS/乙醇溶液灌肠建立大鼠TNBS结肠炎模型,造模成功后随机分模型组和EGCG组(浓度分别为25、50、75mg/kg),另设空白对照组。各组按相应剂量EGCG配成2ml灌胃,空白对照组和模型组给予生理盐水灌胃,连续7天。观察大鼠一般情况、进行疾病活动指数(DAI)、结肠大体形态损伤指数(CMDI)、结肠组织病理学(HI)评分;测定结肠组织匀浆丙二醛(MDA)含量、髓过氧化物酶(MPO)活性;免疫组织化学法检测结肠组织Caspase-1的表达;ELISA法检测血清中IL-1β和IL-18的水平。结果:与模型组大鼠相比,EGCG 75mg/kg浓度时,大鼠一般状况改善,DAI、CMDI和HI评分均有不同程度降低,结肠组织匀浆中MPO活性和MDA含量也有不同程度下降,免疫组化显示结肠组织中Caspase-1表达下降,血清中IL-1β和IL-18浓度也有所降低。结论:EGCG能减轻TNBS结肠炎大鼠结肠炎症,可能与EGCG抑制结肠组织中Caspase-1的表达,降低血清中IL-1β和IL-18的水平相关。
Objective: To observe the therapeutic effect of epigallocatechin-3-gallate (EGCG) on TNBS colitis in rats and explore its possible anti-inflammatory mechanism. Methods: TNBS / ethanol enema was used to establish a model of TNBS colitis in rats. The rats were randomly divided into model group and EGCG group (25, 50 and 75 mg / kg, respectively) after successful modeling. Another blank control group was established. Each group was dosed according to the corresponding dose of EGCG 2ml, blank control group and model group were given saline for 7 days. The general condition of the rats was observed, and the index of disease activity (DAI), gross morphology damage index (CMDI) and histopathology (HI) of the colon were measured. The content of malondialdehyde (MDA) (MPO) activity. The expression of Caspase-1 in colonic tissue was detected by immunohistochemistry. The levels of IL-1β and IL-18 in serum were detected by ELISA. Results: Compared with the model group, the general condition of rats improved at 75mg / kg EGCG, the scores of DAI, CMDI and HI were decreased to some extent, the activity of MPO and the content of MDA in the colonic tissue were also decreased to some extent, Immunohistochemistry showed that the expression of Caspase-1 in colonic tissue was decreased, and the concentrations of IL-1β and IL-18 in serum were also decreased. CONCLUSION: EGCG can relieve colitis in rats with TNBS-induced colitis, which may be related to the inhibition of EGCG expression of Caspase-1 and the decrease of serum IL-1β and IL-18.