The estrogen-like protective effect of ginsenoside Rb3 on oxidative stress and dysfunction of endothelial cells induced by oxidized low-density lipoprotein.
- Author:
Yu-ting PAN
1
;
Chun-yu GUO
;
Xiao-juan MA
;
Jing-shang WANG
;
Xin LIU
;
Ming-yue SUN
;
Miao ZHANG
;
Hui-jun YIN
Author Information
1. Gansu University of Traditional Chinese Medicine, Lanzhou, China.
- Publication Type:Journal Article
- MeSH:
Cells, Cultured;
Endothelial Cells;
drug effects;
Endothelin-1;
metabolism;
Estradiol;
analogs & derivatives;
Estrogens;
pharmacology;
Ginsenosides;
pharmacology;
Humans;
Lipoproteins, LDL;
adverse effects;
Nitric Oxide Synthase Type II;
metabolism;
Nitric Oxide Synthase Type III;
metabolism;
Oxidative Stress;
Panax;
chemistry;
Phosphorylation;
Saponins;
pharmacology;
Superoxide Dismutase;
metabolism
- From:
Acta Pharmaceutica Sinica
2014;49(10):1406-1412
- CountryChina
- Language:Chinese
-
Abstract:
Ginsenoside Rb3 (GRb3) is one of the main components in plasma of Panax quinquefolius Saponin of stem and leaf (PQS), which can be into human plasma. Previous studies have found PQS has estrogen-like vascular protective effects. In the present study, we investigated the estrogen-like protective effect of GRb3 on oxidative stress and dysfunction of endothelial cells induced by oxidized low-density lipoprotein. The activities of SOD, NOS and the contents of MDA in the cell lysate were examined by enzyme method or spectrophotometry. The NO and ET-1 concentrations in the cell culture supernatant were measured by ELISA method. The iNOS and eNOS mRNA expression were measured by real time RT-PCR, while the phosphorylation levels of Akt was measured by Western blotting. The results showed that GRb3 could enhance the activity of SOD, reduce the content of MDA, increase the level of NOS, NO, ET-1 and iNOS mRNA expression while decrease the eNOS mRNA expression and the phosphorylation level of Akt. These effects were blocked by estrogen receptor antagonist ICI182780. GRb3 can play a role in protecting vascular endothelial cells by estrogen receptors, the protective mechanism is similar to 17-β estrodiol.
