Involvement of TLR4/NLRP3 inflammasome in contrast medium-induced inflammation and injury in renal tubular epithelial cells
10.3969/j.issn.1000-4718.2017.12.022
- VernacularTitle:TLR4/NLRP3炎症复合体介导对比剂诱导的 肾小管上皮细胞炎症和损伤
- Author:
Yan LIN
1
;
qiong Jia LIN
;
li Chu XIE
;
feng Xiao GUAN
;
xian Xue TAN
;
na Ze HUANG
Author Information
1. 广州医科大学附属第三医院 肾内科
- Keywords:
Contrast media;
Kidney injury;
Inflammation;
Toll-like receptor 4;
Nod-like receptor protein 3 inflammasome
- From:
Chinese Journal of Pathophysiology
2017;33(12):2252-2258
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate whether Toll-like receptor 4 ( TLR4 ) and Nod-like receptor protein 3 (NLRP3) inflammasome were involved in contrast medium (CM)-induced inflammation and injury in renal tubular epithe-lial cells.METHODS: Iopromide was used to injure NRK-52E cells in the study.The cell viability was measured by CCK-8 assay.The protein levels of TLR4, NLRP3, apoptosis-associated speckle-like protein (ASC), caspase-1 and cleaved caspase-3 were determined by Western blot .The releases of interleukin ( IL )-1βand IL-18 were detected by ELISA .The apoptotic rate was evaluated by Hoechst staining , and mitochondrial membrane potential ( MMP) was analyzed by JC-1 staining.siRNA was transfected into the NRK-52E cells to silence NLRP3 expression.RESULTS:CM decreased the viability of NRK-52E cells (P<0.05).CM also elevated the protein levels of cleaved caspase-3, TLR4, NLRP3, IL-1βand IL-18 (P<0.05).Silencing NLRP3 attenuated CM-induced releases of inflammatory cytokines .Moreover, treat-ment with TLR4 inhibitor TAK-242 or knockdown of NLRP3 by siRNA transfection both attenuated cell apoptosis and loss of MMP caused by CM .CONCLUSION:TLR4/NLRP3 inflammasome takes part in the pathogenesis of CM-induced acute kidney injury , and mediates CM-induced injury and inflammation in renal tubular epithelial cells .
