Objective: To investigate the protective effect of oxymatrine (OMT) on rat primary cardiomyocyte injury induced by transforming growth factor-β1 (TGF-β1)

and explore its mechanism. Method: Primary cardiomyocytes of SD neonatal rats were isolated by trypsin digestion method and purified by differential adhesion method.The cardiomyocytes was divided into four groups

such as the normal group

model group (TGF-β1

20×10-5 g · L-1)

OMT high-dose group (TGF-β1+0.1 g · L-1 OMT) and OMT low-dose group (TGF-β1+0.05 g · L-1 OMT).After being preincubated with OMT for 2 h

and then TGF-β1was added to establish myocardial cell injury model by coculture for 48 h.MTT method was adopted to detect cell viability

and the external leakage of lactate dehydrogenase was analyzed by biochemical method

Western blot was used to detect p38

extracellular signal-regulated protein kinases (ERK) and c-Jun N-terminal kinase (JNK) protein expression levels. Result: TGF-β1 significantly induced cardiomyocyte injury

cardiomyocyte viability decrease and LDH leakage increase were significantly attenuated by OMT with dose of 0.1

0.05 g · L-1.OMT (0.1 g · L-1) could inhibit the expression of p-p38

p-JNK

p-ERK1/2 in myocardium induced by TGF-β1;but it had no effect on total protein expression of p38

JNK and ERK1/2. Conclusion: OMT has protective effect on cardiomyocyte injury induced by TGF-β1

and its mechanism may be involved in inhibiting phosphorylation of p38

ERK1/2 and JNK protein.