文献类型：期刊文献

英文题名：Peroxiredoxin 6 alleviates high glucose-induced inflammation and apoptosis in HK-2 cells by inhibiting TLR4/NF-ΚB signaling

作者：Wu, Hao[1];Wu, Rong[2];Liu, Tianxi[2];Ma, Hongbin[1];Xue, Guozhong[1];Liu, Minglong[2]

第一作者：吴颢

通信作者：Wu, R[1]

机构：[1]Gansu Univ Chinese Med, Affiliated Hosp, Dept Nephrol, Lanzhou, Peoples R China;[2]Lanzhou Univ, Hosp 1, Dept Nephrol, 1 Donggang West Rd, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学第二附属医院

通信机构：[1]corresponding author), Lanzhou Univ, Hosp 1, Dept Nephrol, 1 Donggang West Rd, Lanzhou 730000, Peoples R China.

年份：2023

外文期刊名：ANNALS OF TRANSLATIONAL MEDICINE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000916655100001)】；

语种：英文

外文关键词：Diabetic nephropathy (DN); peroxiredoxin 6; inflammation; apoptosis; TLR4; NF-KB signaling

摘要：Background: This research sought to elucidate the effects of peroxiredoxin 6 (PRDX6) on the biological processes in diabetic nephropathy (DN) and to identify the underlying regulatory mechanism related to toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-KB) signaling.Methods: To induce an in vitro DN cellular model, human kidney 2 (HK-2) cells were treated with high glucose (HG). The mitochondrial membrane potential, adenosine triphosphate level, reactive oxygen species generation, and oxidative stress of the cells were then evaluated. After the PRDX6level had been determined, the effects of its overexpression on the mitochondrial membrane potential, adenosine triphosphate level, reactive oxygen species generation, and oxidative stress of the cells were assessed. Next, cytochrome c expression, cell viability, cell apoptosis, the inflammatory level, and the TLR4/NF-KB signaling-related factors were assessed. After the addition of the TLR4 activator CRX-527 or the NF-KB activator phorbol 12-myristate 13-acetate (PMA), cell viability, cell apoptosis and the inflammatory level were evaluated again.Results: The results revealed that HG exposure triggered mitochondrial dysfunction and oxidative stress and decreased PRDX6 expression in the HK-2 cells. PRDX6 elevation exacerbated cell viability while alleviating mitochondrial membrane potential loss, oxidative stress, apoptosis, and inflammation in the HG-treated HK-2 cells. Further, PRDX6 inhibited HG-induced TLR4/NF-KB activation. The administration of CRX-527 or PMA reversed the effects of PRDX6 on the cell viability, apoptosis, and inflammation of the HG-exposed HK-2 cells.Conclusions: To conclude, PRDX6 appears to protect HG-exposed HK-2 cells against inflammation and apoptosis by inhibiting TLR4/NF-KB signaling.