SchA ameliorates endothelial dysfunction caused by oxidative stress
- VernacularTitle:五味子甲素改善氧化应激引起的内皮功能障碍
- Author:
Hui-min HOU
1
;
Wen-wen ZHANG
1
;
Wei-ping ZHAO
1
;
Xin ZHAO
1
;
Xian-mei PIAO
1
Author Information
- Publication Type:Journal Article
- Keywords: SchA; oxidative stress; endothelial dys-function; Nrf2/Keap1/HO-1 signaling pathway; HU-VECs; LPS
- From: Chinese Pharmacological Bulletin 2025;41(1):122-130
- CountryChina
- Language:Chinese
- Abstract: Aim To investigate the antagonistic effect of Schizandrin A(SchA)on oxidative stress-induced endothelial dysfunction and its mechanism of action.Methods Human umbilical vein endothelial cells(HUVECs)were selected as the research subjects,and the effects of SchA on cell viability were detected by MTT assay;the content of ROS in the cells was detec-ted by flow cytometry;the content of MDA and CAT in the cells,and the content of NO and ET-1 in the cell supernatant were detected by kit assay;and the expres-sion of SOD1,p-eNOS/eNOS proteins,and ET-1 in the cell supernatant were detected by Western blot.Immu-nofluorescence experiments were performed to detect Nrf2 entry into the nucleus of cells.Results SchA re-versed the LPS-or hypoxia-induced increase in ROS and MDA content as well as the decrease in SOD1 and CAT content in HUVECs by activating the Nrf2/Keap1/HO-1 signaling pathway.SchA inhibited the decrease of p-eNOS and eNOS protein expression in HUVECs cells,as well as NO content in cell culture medium and the increase of ET-1 content induced by LPS.The Nrf2 inhibitor ML385 reversed the antagonis-tic effects of SchA on oxidative stress and endothelial dysfunction.Conclusions SchA antagonized LPS and hypoxia-induced oxidative stress,and SchA amelio-rated oxidative stress-induced endothelial dysfunction by up-regulating the Nrf2/Keap1/HO-1 signaling path-way.
