Objective: To investigate the protective effect of oxymatrine(OMT) on cardiac myocytes injure induced by aldosterone and explore its mechanism. Method: The cardiomyocytes of neonatal rats were isolated and purified by trypsin digestion and differential adherence method for culture

and then 1×10-5mol·L-1 ALD was used to establish myocardial injury models. The experiment was divided into blank group

model group (1×10-5mol·L-1 ALD)

ALD+OMT high dose group (3.78×10-4 mol·L-1)

ALD+OMT low dose group (1.89×10-4 mol·L-1)

ALD+JNK inhibitor group (JNK I

5×10-6mol·L-1)

ALD+Aspirin group (Asp

1×10-5 mol·L-1). That is to say

in OMT

JNK inhibitor and Aspirin groups

after pre-treatment with corresponding medicines for 2 h

ALD with the final concentration of 1×10-5 mol·L-1 was added for co-incubation for 24 h. Then MTT assay was used to detect the cell survival rate; the morphological changes of cardiac myocytes were observed by Giemsa staining; Western blot and Real-time PCR were used to analyze the effect of OMT on the protein and mRNA expression of JNK and p-JNK. Result: As compared with the blank group

ALD significantly reduced the survival rate of cardiac myocytes(P<0.01) and changed the cell morphology; OMT could reverse the decrease in survival rate of cardiac myocytes(P<0.01) and restore the cells to normal form; Western blot showed that ALD could increase the phosphorylation of JNK (P<0.01)

while the expression of p-JNK was significantly down-regulated after pre-incubated with OMT as compared with ALD group (P<0.01). Real-time PCR results showed that the expression of JNK mRNA in ALD group was higher than that in normal control group (P<0.01)

however no significant change of gene expression was observed in OMT group. Conclusion: OMT had protective effect on ALD-induced cardiac myocytes injury

and its mechanism may be closely related to inhibiting JNK protein phosphorylation.