RESUMO
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.