地黄梓醇对高糖介导足细胞焦亡的抑制作用及机制研究  

Study on the Mechanism and Inhibitory Effect of Catalpol on High Glucose-induced Podocyte Pyroptosis

作　　者：陈慧[1] 杨洪涛[2] 许正锦[1] 周燕妮 吴玲艳[1] 王海烨 许勇镇 CHEN Hui;YANG Hongtao;XU Zhengjin(Department of Nephrology,Xiamen Hospital of Chinese Medicine,Xiamen 361000)

机构地区：[1]厦门市中医院肾病科,厦门361000 [2]天津中医药大学第一附属医院肾病科,天津300000

出　　处：《中国中西医结合肾病杂志》2023年第11期953-956,共4页Chinese Journal of Integrated Traditional and Western Nephrology

基　　金：厦门市医疗卫生指导性项目(No.3502Z20214ZD1160)。

摘　　要：目的:探讨地黄梓醇对高糖介导足细胞焦亡的作用及其机制。方法:用高糖刺激小鼠足细胞建立细胞焦亡模型,不同浓度的地黄梓醇预给药,分为对照组、高糖组、地黄梓醇处理组。用CCK8法测定细胞活力;流式细胞仪检测细胞焦亡情况及足细胞ROS水平;Western blot法测定NLRP3、Active-caspase1、GSDMD-N蛋白表达;ELISA法测定细胞上清液IL-1β、IL-18水平。结果:地黄梓醇能抑制高糖介导的足细胞焦亡及ROS水平升高;地黄梓醇能减少高糖导致的小鼠足细胞NLRP3、Active-caspase1、GSDMD-N蛋白水平升高及IL-1β、IL-18释放增多。结论:地黄梓醇可通过抑制ROS-NLRP3-Caspase1通路来抑制小鼠足细胞焦亡。Objective:To investigate the mechanism and effect of catalpol on high glucose(HG)-induced podocyte pyroptosis.Methods:The mouce podocytes were sitimulated with HG to establish pyroptosis model.The podocytes were pre-administered with different concentrations of catalpol and divided into control group,HG group and catalpol treatment group.Cellular viability was detected by CCK8.The cell pyroptosis and ROS levels of podocytes were tested by flow cytometry.The protein expressions of NLRP3、Active-caspase1 and GSDMD-N were detected by western blot.Interleukin-1β(IL-1β) and interleukin-18(IL-18) levels were detected by ELISA.Results:Catalpol significantly decreased pyroptosis and ROS generation of podocytes induced by HG.Catalpol significantly decreased levels of NLRP3,Active-caspase1,GSDMD-N,IL-1β and IL-18 in podocytes induced by HG.Conclusion:Catalpol inhibits HG-induced podocyte pyroptosis by Inhibiting ROS-NLRP3-caspase1 pathway.

关 键 词：地黄梓醇 足细胞 细胞焦亡 

分 类 号：R285[医药卫生—中药学]