NLRP3炎症小体在高糖诱导小鼠肾小管上皮细胞EMT中的作用

Role of NLRP3 Inflammsome in Epithelial-mesenchymal Transition Induced by High Glucose in Mouse Renal Tubular Epithelial Cell

目的:观察NLRP3炎症小体在高糖诱导小鼠肾小管上皮细胞上皮间质转化(EMT)中的作用。方法:以小鼠肾小管上皮细胞为研究对象,高糖处理24h后,采用real-time PCR法检测细胞表型标志分子(E钙粘素和α-SMA)和NLRP3炎症小体mRNA的表达,ELISA法检测细胞上清液中IL-1β含量。采用NLRP3炎症小体特异性抑制剂MCC950探讨NLRP3炎症小体在高糖诱导小鼠肾小管上皮细胞ETM中的作用。结果:高糖处理24h可降低小鼠肾小管上皮细胞E钙粘素mRNA表达,上调α-SMA mRNA表达;同时上调NLRP3、pro-IL-1β和pro-caspase-1 mRNA表达,以及IL-1β分泌;抑制NLRP3炎症小体可部分逆转高糖诱导的小鼠肾小管上皮细胞EMT。结论:高糖应激可能通过激活NLRP3炎症小体促进IL-1β分泌诱导肾小管上皮细胞发生EMT。

Objective：To observe the effect of NLRP3 inflammasome on epithelial-mesenchymal transition （EMT） induced by high glucose in mouse renal tubular epithelial cells. Methods：Mouse renal tubular epithelial cells were used in this study. The expressions ofE-cadherin and α-SMA and NLRP3 inflammasome were detected by real-time PCR. The content of IL-1β in supernatant wasdetected by ELISA. A specific inhibitor of NLRP3 inflammsome MCC950 was used to investigate the role of NLRP3 inflam- masome in EMT induced by high glucose in mouse renal tubular epithelial cells. Results： The expression of E-cadherin mRNA in mouse renal tubular epithelial cells was inhibited by high glucose for 24 h,and the expression of α SMA mRNA was up-regulated. High glucose treatment also increased the expressions of NLRP3 ,pro-IL-1β and pro-caspase-1 mRNA and IL-1β secretion. Inhibition of NLRP3 inflammasome can partially reverse the high glucose-induced EMT in mouse renal tubular epithelial cell. Conclusion： High glucose may promote the development of EMT in renal tubular epithelial cells induced by IL-1β via activating NLRP3 inflammasome.