Oxymatrine improves palmitic acid-induced vascular endothelial cell injury through Akt-eNOS-NO signaling pathway
- Author:
Xin SONG
1
;
Ya-Ping LIU
1
;
Yu-Hao WANG
1
;
Jia-Quan ZHU
1
;
Jin-Fu WEN
1
;
Xin SONG
2
;
Ya-Ping LIU
2
;
Yu-Hao WANG
2
;
Jia-Quan ZHU
2
;
Song-Nan JIN
2
;
Jin-Fu WEN
3
Author Information
- Publication Type:Journal Article
- Keywords: Akt; endothelial nitric oxide synthase; human umbilical vein endothelial cells; nitric oxide; oxymatrine; palmitic acid
- From: Chinese Pharmacological Bulletin 2023;39(3):525-531
- CountryChina
- Language:Chinese
- Abstract: Aim To investigate the protective effect of oxymatrine (OMT) on vascular endothelial cell injury induced by palmitic acid ( PA) and its mechanism. Methods Cell viability was detected by MTT assay. Cell apoptosis was detected by flow cytometry. The levels of oxygen species ( ROS) in cells, and lactate de-hydrogenase, malondialdehyde (MDA), superoxide dismutase (SOD) , glutathione peroxidase (GSH-PX) and nitric oxide ( NO) in cell culture medium were detected by ELISA. The protein expressions of bcl-2, bax, caspase-3, Akt and eNOS in HUVECs were detected by Western blot. Results OMT significantly inhibited PA-induced decrease in cell viability and increase in level of LDH in HUVECs. OMT also significantly inhibited PA-induced increase in cell apoptosis, and up-regulated the protein expression ratio of bcl-2/ bax and down-regulated the protein expression of caspase-3. In addition, OMT reduced the levels of ROS and MDA, and increased the levels of SOD, GSH-Px and NO in cell-culture medium treated with PA. Furthermore, OMT increased the protein phospho-rylation of Akt and eNOS in injured cells. Conclusion OMT ameliorates PA-induced vascular endothelial cell injury through Akt-eNOS-NO signaling pathway.
