Salvianic acid A inhibits lipopolysaccharide-induced apoptosis through regulating glutathione peroxidase activity and malondialdehyde level in vascular endothelial cells.
10.1016/S1875-5364(12)60012-0
- Author:
Qi-Tao ZHAO
1
;
Qing-Mei GUO
;
Peng WANG
;
Qian WANG
Author Information
1. Laboratory of Cytobiology, School of Basic Medicine, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
- Publication Type:Journal Article
- MeSH:
Antioxidants;
pharmacology;
Apoptosis;
drug effects;
Cell Cycle;
drug effects;
Cell Line;
Cell Survival;
drug effects;
Dose-Response Relationship, Drug;
Drugs, Chinese Herbal;
pharmacology;
Endothelium, Vascular;
cytology;
drug effects;
metabolism;
Glutathione Peroxidase;
metabolism;
Human Umbilical Vein Endothelial Cells;
Humans;
Lactates;
pharmacology;
Lipopolysaccharides;
Malondialdehyde;
metabolism;
Salvia miltiorrhiza;
chemistry
- From:
Chinese Journal of Natural Medicines (English Ed.)
2012;10(1):53-57
- CountryChina
- Language:English
-
Abstract:
AIM:To find out the role of salvianic acid A (SAA) in the protection of vascular endothelial cells (VEC) and its possible mechanism in vitro.
METHODS:The ingredient at various concentrations was added to human umbilical vein endothelial cells (HUVEC) treated with 0.5 μmol·L(-1) lipopolysaccharide (LPS) for 24 h. Apoptotic morphological changes of cells were observed under inverted phase contrast microscope; the cell viability was quantified using MTT assay. Nuclear fragmentation of cells was observed under laser scanning confocal microcope after being stained with acridinorange. Cell cycle distribution was detected by flow-cytometry after being stained with propidium iodide (PI). The activities of glutathione peroxidase (GPH-PX) as well as maleic dialdehyde (MDA) level in cells were measured by spectrophotometric methods as described in the assay kits.
RESULTS:Apoptotic morphological changes and the decrease of cell viability of these cells were obviously inhibited by SAA in a dose-dependent manner. Furthermore, the abnormal cell cycle distribution, the decrease of GSH-Px activity and the increase of MDA level induced by LPS were markedly reversed.
CONCLUSION:SAA exerts protective effect on VEC induced by LPS via an antioxidative mechanism.
