Effect of ERK1/2 signaling pathway on astragaloside IV protects H9c2 cells against H2O2-induced oxidative injury.
- Author:
Yuan-yuan WANG
1
;
Yang PENG
;
Qi ZHANG
;
Yan-na WU
;
Jun-qiu SONG
;
Yan-xia LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antioxidants; pharmacology; Cell Line; Hydrogen Peroxide; toxicity; MAP Kinase Signaling System; physiology; Myoblasts, Cardiac; drug effects; metabolism; pathology; Oxidative Stress; drug effects; Protective Agents; pharmacology; Rats; Saponins; pharmacology; Triterpenes; pharmacology
- From: Chinese Journal of Applied Physiology 2011;27(3):363-367
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether Astragaloside IV(AST) protects H9c2 cells against H2O2-induced oxidative injury partly through ERK1/2 signaling pathway.
METHODSH9c2 cells oxidative injury was induced by 200 tmol/L H2O2 for 6 hours to establish the H2O2-induced injury model of H9c2 cells. The viability of H9c2 cells was detected using MTf method. Activity of lactate dehydrogenase(LDH), total-superoxide dismutase (T-SOD), manganese-superoxide dismutase (Mn-SOD) and content of MDA (malondialdehyde) in the culture medium were detected using colorimetric method. Western blot was performed to exam expression of p-ERK1/2 and ERK1/2 in H9c2 cells respectively.
RESULTSUnder 200 micromol/L H2O2 treatment for 6 hours, the vaibility of H9c2 cells was suitable for the following study. Compared with H2O2 group, the cell viability was increased significantly in AST10 + H2O2 and AST2O + H2O2 groups (P < 0.01). The activity of LDH in the culture medium was decreased significantly (P < 0.01). The activity of T-SOD and Mn-SOD was increased significantly (P < 0.01), the content of MDA was decreased significantly (P < 0.01). Treated with 10 mg/L or 20 mg/L of AST, expression of p-ERK1/2 in H9c2 cells injured from H2O2 was increased significantly (P < 0.01), when PD98059 (inhibitor of ERK1/2) was added, the effects of AST were cancelled.
CONCLUSIONAST protects H9c2 cells against H2O2-induced oxidative injury partly through ERK1/2 signaling pathway.