Acanthopanax senticosus saponins ameliorates oxidative damage induced by hydrogen peroxide in neonatal rat cardiomyocytes.
- Author:
Qiming LIANG
1
;
Shaochun QU
;
Xiaofeng YU
;
Huali XU
;
Dayun SUI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Catalase; metabolism; Cells, Cultured; Drugs, Chinese Herbal; pharmacology; Eleutherococcus; chemistry; Female; Glutathione Peroxidase; metabolism; Hydrogen Peroxide; pharmacology; Male; Myocytes, Cardiac; drug effects; enzymology; metabolism; Oxidative Stress; drug effects; Rats; Rats, Wistar; Saponins; pharmacology; Superoxide Dismutase; metabolism
- From: China Journal of Chinese Materia Medica 2009;34(19):2489-2493
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of Acanthopanax senticosus saponins (ASS) on oxidative damage induced by hydrogen peroxide (H2O2 ) in cardiomyocytes.
METHODThe cardiomyocytes were induced to oxidative damaged by exposed to H2O2. We evaluated the level of oxidative injury through morphology change, the survival rate, the activity of lactate dehydrogenase (LDH) and the content of cellular malondialdehyde (MDA). The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and the content of reductive glutathione (GSH) of cardiomyocytes were also determined.
RESULTWhen the cardiomyocytes were exposed to H2O, (50, 100, 200 micromol x L(-1)) for deigned time, the percentage of survival cells was down significantly (P < 0.01 or P < 0.001), and the activity of LDH and the content of MDA were increased markedly (P < 0.05, P < 0.01 or P < 0.001). These results show that the cells were subjected to oxidative damage. Treatment with ASS (600 mg x L(-1)) prior to H2O2 exposure could increase cell viability significantly, lessen cardiomyocyte morphological damaged change, and decrease LDH activity (1687.40 +/- 97.51) U x mL(-1) in media and cellular MDA content (16.50 +/- 2.66) nmol x mg(-1) markedly (P < 0.01 and P < 0.05). Furthermore, the activities of SOD (89.55 +/- 6.93) U x mg(-1), GSH-Px (845.87 +/- 63.76) mU x mg(-1), CAT (93.07 +/- 10.40) U x mg(-1) and the content of GSH (8.91 +/- 1.06) micromol x mg(-1) of cardiomyocytes were also raised by 600 mg x L(-1) l ASS (P < 0.05).
CONCLUSIONTaken together, the study implicate that ASS protects cardiomyocytes against oxidative-stress injury induced by H2O2 through reduction of lipid peroxidation and enhancement of the activity of antioxidant defense.