Knockdown of NLRC5 attenuates renal I/R injury in vitro through the activation of PI3K/Akt signaling pathway

• Published in: Biomedicine & pharmacotherapy 2018-07, Vol.103, p.222-227
• Main Authors: Han, Feng, Gao, Yi, Ding, Chen-guang, Xia, Xin-xin, Wang, Yu-xiang, Xue, Wu-Jun, Ding, Xiao-Ming, Zheng, Jin, Tian, Pu-Xun
• Format: Article
• Language: English
• Subjects: Apoptosis; Kidney injury; NLRC5; Oxidative stress
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2018.04.040

[Display omitted] •NLRC5 is upregulated in HK-2 cells subjected to H/R.•Knockdown of NLRC5 improves the viability of HK-2 cells exposed to H/R.•Knockdown of NLRC5 inhibits H/R-induced oxidative stress in HK-2 cells.•Knockdown of NLRC5 inhibits H/R-induced HK-2 cell apoptosis.•Knockdown of NLRC5 enhances PIK3/Akt activation in H/R-stimulated HK-2 cells. NLRC5, as the largest member of nucleotide-binding domain and leucine-rich repeat (NLR) family, was involved in various physiological processes, such as inflammation, fibrosis, innate immunity and diabetic nephropathy. However, the role of NLRC5 in acute kidney injury remains unclear. The aim of this study was to investigate the role of NLRC5 in human renal proximal tubular epithelial cells (HK-2) exposed to hypoxia/reoxygenation (H/R). Our results demonstrated that the expression of NLRC5 was significantly up-regulated in HK-2 cells exposed to H/R. Knockdown of NLRC5 significantly improved the viability of HK-2 cells exposed to H/R. In addition, knockdown of NLRC5 efficiently inhibited H/R-induced oxidative stress and apoptosis in HK-2 cells. Mechanistically, knockdown of NLRC5 markedly enhanced the activation of PIK3/Akt signaling pathway in H/R-stimulated HK-2 cells. In summary, our findings indicate that knockdown of NLRC5 attenuates renal I/R injury in vitro through the activation of PI3K/Akt signaling pathway.