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目的:研究18β-甘草次酸(GA)对脂多糖诱导的IEC-6肠上皮细胞损伤的保护作用。方法:将IEC-6细胞与LPS(100μg.mL1)和不同浓度的GA(0.1,1.0,10μmol.L1)共孵24h后,观察GA的保护作用。ELISA检测细胞因子TNF-α和IL-6的水平;亚硝酸盐分析法测量上清中NO的含量;流式细胞术检测ROS的水平;TER检测肠上皮细胞通透性;Westernblotting分析ZO-1,COX-2和PGDH蛋白表达水平。结果:GA可以抑制由脂多糖刺激IEC-6细胞产生的TNF-α和IL-6的水平,降低ROS和NO,部分恢复肠上皮细胞的通透性,显著提高紧密连接相关蛋白ZO-1的表达量,同时下调COX-2的表达量,而上调PGDH的表达量。结论:GA能减轻由脂多糖引发的肠上皮细胞的损伤,并且能保护肠上皮细胞的紧密连接,其中的机制和炎症因子的下调以及对COX-2和PGDH的调节有关。
Objective: To study the protective effect of 18β-glycyrrhetinic acid (GA) on lipopolysaccharide-induced injury of IEC-6 intestinal epithelial cells. Methods: IEC-6 cells were incubated with LPS (100μg.mL1) and different concentrations of GA (0.1,1.0,10μmol.L1) 24h after incubation, observe the protective effect of GA. ELISA was used to detect the levels of cytokines TNF-α and IL-6; NO was measured by nitrite assay; the ROS level was detected by flow cytometry; the permeability of intestinal epithelial cells was detected by TER; , COX-2 and PGDH protein expression levels. Results: GA could inhibit the level of TNF-α and IL-6 produced by IEC-6 cells stimulated by lipopolysaccharide, reduce ROS and NO, partially restore the permeability of intestinal epithelial cells and significantly increase the expression of tight junction-associated protein ZO-1 While down-regulating the expression of COX-2 and up-regulating the expression of PGDH. CONCLUSION: GA can reduce the damage of intestinal epithelial cells induced by lipopolysaccharide and protect the intestinal epithelial cells from tight junction. The mechanisms involved are downregulation of inflammatory factors and regulation of COX-2 and PGDH.