Mechanism of NLRP3 inflammasome activation caused by albumin in renal tubulointerstitial cells
10.13315/j.cnki.cjcep.2017.12.011
- VernacularTitle:白蛋白导致肾小管上皮细胞NLRP3炎性体激活的机制分析
- Author:
Li-Hong DING
1
;
Lin-Li L(U)
;
De-Guang WANG
;
Li HAO
Author Information
1. 安徽医科大学第二附属医院肾内科
- Keywords:
albumin;
NLRP3 inflammasome;
Cathepsin B;
reactive oxygen species
- From:
Chinese Journal of Clinical and Experimental Pathology
2017;33(12):1341-1345
- CountryChina
- Language:Chinese
-
Abstract:
Purpose To study the mechanism of NLRP3 inflammasome activation caused by albumin in renal tubulointerstitial cells.Methods Cathepsin B was detected by immunohistochemistry in renal biopsy tissue of 30 membranous nephropathy patients which had different levels of proteinuria.HK-2 cells were stimulated by albumin,and then were treated by high concentration KCl,CA 074 Me and DPI,which was Cathepsin B inhibitor and ROS inhibitor.Finally,IL-1β and IL-18 were detected by Western blot and real time PCR,respectively.Results The expression of Cathepsin B in tubulointerstitial cells was significantly higher in patients with severe proteinuria than that in patients with mild proteinuria (P ＜ 0.05).CA 074 Me and DPI significantly reduced IL-1β and IL-18 secretion in HK-2 cells stimulated by albumin (P ＜ 0.05),but high concentration KCl did not result in this change (P ＞ 0.05).Conclusion NLRP3 inflammasome is activated via Cathepsin B release and increases ROS production caused by proteinuria,but not via K + efflux.
