Objective: To preliminarily investigate the protective effects of quercetin on the survival rate of H2O2-induced oxidative injury in H9C2 cardiomyocytes

and such key factors as reactive oxygen species (ROS)

nicotinamide adenosine denucleotide hydro-phosphoric acid(NADPH) oxidase and apoptosis

in order to clarify the underlying mechanism. Method: A model of hydrogen peroxide H2O2-induced H9C2 cells oxidative injury was established in vitro

and divided into the normal group

the model group and the quercetin group. Cell viability was examined with an methylthiazolyldiphenyl-tetrazolium bromide(MTT) assay to determine the available concentrations of H2O2 and quercetin. The effects of quercetin on ROS level and apoptosis rate were detected by 2'

7'-Dichloroflurescin diacetate (DCFH-DA) and flow-cytometry

respectively. We also used Real-time PCR and Western blot to examine the effect of quercetin on oxidative stress and apoptosis mechanism-related molecules (NOX-4

p22phox

Bcl-2

Bax and Caspase-8)genes and protein expression level. Result: Quercetin of 10 μmol·L-1 has significant anti-oxidative and anti-apoptotic effect. Cell survival rate increased obviously in quercetin group compared with H2O2-model group (P<0.05)

ROS level and apoptosis rate significantly decreased (P<0.05

P<0.01). Moreover

quercetin had an up-regulation on PI3K

Bcl-2 and NOX4 (P<0.05) and down-regulation of p22phox

Bax and Caspase-8 (P<0.05). Meanwhile

quercetin can inhibit Bax

p22phox protein expressions (P<0.05)

and up-regulate PI3K

Bcl-2 protein expressions (P<0.05). Conclusion: Quercetin protects H9C2 cells from H2O2-induced oxidative injury and inhibit myocardial cell apoptosis by regulating NOX-4 p22phox

reducing intracellular ROS level

activating PI3K and increasing Bcl-2.