[Inhibitory effect of sinomenine on H2O2-induced apoptosis in neonatal rat cardiomyocytes].
OBJECTIVE
To study the effects of sinomenine on apoptosis in cutured neonatal rat cardiomyocytes induced by H2O2 and its possible mechanism.


METHODS
H2O2 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.


RESULTS
Compared 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)).


CONCLUSIONS
Sinomenine 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.
Li
Le
L
School of Pharmacy, Zhejiang University of Technology, Hangzhou 310014, China. lile_1856@163.com
Gao
Xiao-Li
XL
Ding
Bao-Xin
BX
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D005786:Gene Expression Regulation / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000633:toxicity*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D009019:Morphinans / Q000494:pharmacology*; D032383:Myocytes, Cardiac / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
D009019:Morphinans; D016328:NF-kappa B; D008315:Malondialdehyde; C009271:sinomenine; D006861:Hydrogen Peroxide; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase