Salidroside protects cultured rat subventricular zone neural stem cells against hypoxia injury by inhibiting Bax, Bcl-2 and caspase-3 expressions.
- Author:
Cunfang QI
1
;
Junfeng ZHANG
;
Xinlin CHEN
;
JiansHui ZHANG
;
Pengbo YANG
;
Qian JIAO
;
Pengbo ZHANG
;
Hai-Xia LU
;
Yong LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Caspase 3; metabolism; Cell Hypoxia; Cells, Cultured; Flow Cytometry; Glucosides; pharmacology; Neural Stem Cells; drug effects; Phenols; pharmacology; Proto-Oncogene Proteins c-bcl-2; metabolism; Rats; Rats, Sprague-Dawley; bcl-2-Associated X Protein; metabolism
- From: Journal of Southern Medical University 2013;33(7):962-966
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effects of salidroside (sal) on the expressions of Bcl-2, Bax and caspases-3 proteins in cultured rat subventricular zone (SVZ) neural stem cells (NSCs) exposed to hypoxia injury.
METHODSPrimarily cultured SVZ NSCs from adult SD rats were incubated with salidroside (120 and 240 µmol/L) for 24 h prior to exposure to hypoxia. The cell viability was assessed with MTT assay, and the cell apoptosis was analyzed using TUNEL staining and flow cytometry. Western blotting was performed to detect the expressions of Bcl-2, Bax and caspase-3 in the cells.
RESULTSSalidroside pretreatment of the cells for 24 h resulted in an obvious resistance to hypoxia-induced cell apoptosis and decrement of cell viability (P<0.05). Salidroside also antagonized the effect of hypoxia exposure in lowering Bcl-2/Bax ratio apoptosis of rat neural stem cells and decreased the expression of caspases-3 protein (P<0.05).
CONCLUSIONSalidroside can significantly resist hypoxia-induced. The neuroprotective effect of salidroside may be related to the modulation of expressions of apoptosis-related proteins.
