Inhibitory effect of sinomenine on H2O2-induced apoptosis in neonatal rat cardiomyocytes.
- Author:
Le LI
1
;
Xiao-Li GAO
;
Bao-Xin DING
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Gene Expression Regulation; drug effects; Hydrogen Peroxide; toxicity; L-Lactate Dehydrogenase; metabolism; Malondialdehyde; metabolism; Morphinans; pharmacology; Myocytes, Cardiac; cytology; drug effects; metabolism; NF-kappa B; metabolism; Rats; Rats, Wistar; Superoxide Dismutase; metabolism
- From: China Journal of Chinese Materia Medica 2008;33(8):939-961
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of sinomenine on apoptosis in cutured neonatal rat cardiomyocytes induced by H2O2 and its possible mechanism.
METHODH2O2 was used to build an oxidative stress-induced injury model in neonatal rat cardiomyocytes after being treated with sinomenine (10, 30, 100 micromol L(-1)), the apoptosis rate, the content of malondialdehyde (MDA), the activity of superoxide dimutase (SOD), the activity of lactate dehydrogenase (LDH) and expression of NF-kappaB protein of the Cardiomyocytes were examined.
RESULTCompared with the model group, the apoptosis rate and the content of MDA, LDH decreased greatly (P < 0.01), and the activity of SOD increased distinctly (P < 0.01) after being treated by sinomenine (10, 30, 100 micromol x L(-1)).
CONCLUSIONSinomenine can inhibit the apoptosis induced by H2O2 in neonatal rat cardiomyocytes. The protective mechanism could be related to its ability to reduce lipid pexosidation and to inhibit cardiomyocyte expression of NF-kappaB protein.
