Effect and Mechanism of Dioscin on Ameliorating Uric Acid-Induced Oxidative Stress Injury in HK-2 Cells Through GSK3β/Nrf2/HO-1 Pathway
10.19378/j.issn.1003-9783.2024.03.005
- VernacularTitle:薯蓣皂苷通过GSK3β/Nrf2/HO-1通路改善尿酸诱导的HK-2细胞氧化应激损伤的作用及机制研究
- Author:
Lijuan ZHOU
1
;
Weiliang ZHANG
;
Ruiqi LIU
;
Jiashu FENG
;
Yingjuan HUANG
;
Xinlin WU
Author Information
1. 中山大学附属第一医院中医科,广东 广州 510080
- Keywords:
dioscin;
uric acid;
HK-2 cells;
GSK3β/Nrf2/HO-1 pathway;
oxidative stress
- From:
Traditional Chinese Drug Research & Clinical Pharmacology
2024;35(3):342-348
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of dioscin on uric acid(UA)-induced oxidative stress injury of human renal tubular epithelial cells(HK-2)and its molecular mechanism.Methods HK-2 cells were cultured and divided into four groups:blank group(normal group),model group(uric acid-stimulation modeling),condition control group(UA+DMSO)and dioscin group(UA+dioscin).Oxidative stress injury model was induced by UA in HK-2 cells.Cells viability was detected by CCK-8.ROS level was detected by flow cytometry.Real-time PCR was used to detect the expressions of glycogen synthase kinase 3β(GSK3β),nuclear factor erythroid 2-related factor 2(Nrf2)and heme oxygenase 1(HO-1)at mRNA level,and Western Blot was used to detect the expressions of phosphorylated glycogen synthesis kinase 3β(p-GSK3β),GSK3β,Nrf2 and HO-1 at protein level.Results After stimulation by UA,HK-2 cells viability was obviously decreased,and ROS level was significantly increased(all P＜0.001).When treated with dioscin,HK-2 cells viability was obviously increased,and the ROS level of HK-2 cells was significantly decreased(all P＜0.001).The expressions of Nrf2 and HO-1 decreased at the protein and mRNA levels after stimulation with UA.But the expressions of Nrf2 and HO-1 significantly increased after treated with dioscin(all P＜0.001).Compared with the blank group,the p-GSK3β/GSK3β ratio in the model group decreased significantly at the protein level,but the p-GSK3β/GSK3β ratio increased after treated with dioscin(all P＜0.001).Conclusion Dioscin can alleviate UA-induced oxidative stress injury in HK-2 cells.The mechanism might be that dioscin can promote phosphorylation of GSK3β,and activate Nrf2/HO-1 pathway.
