Allograft inflammatory factor-1 enhances inflammation and oxidative stress via the NF-κB pathway of bladder urothelium in diabetic rat model

尿路上皮 炎症 NF-κB 氧化应激 肿瘤坏死因子α 下调和上调 αBκ 免疫印迹 癌症研究 化学 细胞生物学 医学 生物 内科学 膀胱 生物化学 基因
作者
Qinguo Wu,Bin Qin,Xiaoyun Wu,Mingjin Zhang,Zhaokai Gan,Yibi Lan,Chunlei Ma,Weijin Fu
出处
期刊:Cytokine [Elsevier BV]
卷期号:173: 156438-156438 被引量:2
标识
DOI:10.1016/j.cyto.2023.156438
摘要

To explore the role of allograft inflammatory factor-1 (AIF-1) both in diabetic rat bladder urothelium and in high-glucose-treated human urothelial cell line (SV-HUC-1). Inflammation and oxidative stress (OS) promote diabetic cystopathy (DCP), but the mechanisms are not fully understood. The expression level of AIF-1 in diabetic rat bladder urothelium and in the SV-HUC-1 cells treated with high glucose was detected using tissue immunofluorescence, immunohistochemistry and western blot assays. AIF-1 was knocked down and NF-κB was suppressed with the specific inhibitor BAY 11–7082 in high-glucose-treated SV-HUC-1 cells. High-glucose condition induced AIF-1 upregulation in vivo and in vitro. The up-regulated AIF-1 induced the production of inflammatory factors IL-6 and TNF-α and elevation of ROS. Informatics analysis suggested that NF-κB pathway is implicated in DCP. Through knockdown of AIF-1, we confirmed that AIF-1 simulated NF-κB pathway by enhancing the phosphorylation of IκB (p-IκB) and promoting the translocation of NF-κB p65 from cytoplasm into nucleus. Additionally, High-glucose-induced inflammation in SV-HUC-1 cells was attenuated by the addition of NF-κB inhibitor. This study provides novel information to understand the molecular regulation mechanisms of AIF-1 in DCP.
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