雷公藤多苷通过线粒体自噬-NLRP3通路干预溃疡性结肠炎的机制分析

The mechanism analysis of tripterygium wilfordii polyglycoside on ulcerative colitis though mitophagy-NLRP3 pathway

目的评价雷公藤多苷对溃疡性结肠炎(UC)的疗效,并探讨其作用机制。方法动物实验:将24只雄性BALB/C小鼠随机分为对照组、UC组、雷公藤多苷药物组,每组8只。UC组及药物组进行UC造模,造模成功后药物组予雷公藤多苷药物治疗,14 d后处死小鼠,取各组病变最严重的结肠组织进行肉眼及组织学检查。细胞实验:将RAW264.7细胞设定对照组、脂多糖(LPS)组、药物组,LPS组及药物组细胞中进行炎症造模,造模成功后药物组予雷公藤红素干预。分别培养24 h后,取细胞培养液,提取细胞蛋白做定量、变性进行分析。结果在动物实验中,雷公藤多苷药物组小鼠DAI评分、结肠病理情况均好于UC组(P<0.05)。细胞实验中,雷公藤红素药物细胞炎症因子及自噬相关蛋白表达均低于LPS组(P<0.05)。结论雷公藤多苷可以改善UC的肠道黏膜损伤,这可能与其抑制线粒体的自噬有关。

Objective To evaluate the effect of tripterygium wilfordii polyglycoside on ulcerative colitis,and to explore its possible mechanism of action.Methods Twenty-four male BALB/C mice were randomly divided into control group,UC group,and drug group,with 8 mice in each group.The UC group and the drug group were subjected to UC modeling.After the successful modeling,the drug group was treated with tripterygium wilfordii polyglycoside.All mice were sacrificed 14 days later,and the most severely diseased colon tissues of each group were taken for visual and histological examination.Cell experiment:The RAW264.7 cells were set up in the control group,LPS group,drug group,LPS group and drug group for inflammation modeling.After the successful modeling,the ceUs of the drug group were treated with tripterine to intervene.After culturing for 24 hours,the cell culture medium was taken,and the cell protein was extracted and analyzed for quantitative and denaturation.Results In animal experiment,the pathology and other conditions of the colon of the mice in the drug group were better than those in the UC group.In the cell experiment,the expressions of inflammatory factors and autophagy-related proteins in the drug group were lower than those in the LPS group.Conclusion Tripterygium wilfordii polyglycosides can improve the intestinal mucosa injury of UC,which may be related to its inhibition of mitochondrial autophagy.