Effects of high concentration of uric acid on oxidative stress and inflammatory response of glomerular endothelial cells

ZHANG Quan; ZHOU Yiyi; FAN Xing; HAN Hongling

doi:10.3969/j.issn.1002-266X.2018.48.013

Abstract：Objective To investigate the effects of high concentration of uric acid on oxidative stress and inflammatory response in glomerular endothelial cells.Methods Human glomerular endothelial cells (HRGECs) subcultured for 5-15times with well condition were inoculated into 6-well plates in this study.HRGECs were randomly divided into four groups:the negative control group, physiological concentration uric acid group, medium concentration uric acid group, and high concentration uric acid group, which were given 0, 4, 8, and 16 mg/d L uric acid for 24 h, respectively.Then, we used real-time PCR and Western blotting to detect the mRNA and protein expression levels of endothelial nitric oxide synthase (e NOS), intercellular adhesion molecule 1 (ICAM-1), monocyte chemotactic protein-1 (MCP-1), and nuclear factor-κB p56 (NF-κB p56).The reactive oxygen species (ROS) content was detected by fluorescent probe method.Results Compared with the medium concentration uric acid group and the high concentration uric acid group, the relative mRNA and protein expression levels of e NOS in the negative control group and the physiological concentration uric acid group significantly decreased (both P＜0.05);the mRNA and protein expression levels of ICAM-1, MCP-1, NF-κB p65, and ROS content significantly increased in the negative control group and the physiological concentration uric acid group (all P＜0.05).However, there was no significant deference in the above parameters between the negative control group, the physiological concentration uric acid group, medium concentration uric acid group and high concentration uric acid group (all P>0.05).ConclusionHigh concentration of uric acid may increase glomerular endothelial cell injury by increasing ROS production and inhibiting e NOS expression in the oxidative stress pathway, and activating NF-κB signaling pathway to promote inflammatory factor secretion.