Objective: To investigate the protective effects of oxymatrine (OMT) on rat primary cardiomyocyte injury induced by aldosterone (ALD)

and explore its effects on transcription and expression of mineralcorticoid receptor (MR). Method: Primary cardiomyocytes of Sprague-Dawley (SD) rats were isolated by trypsin digestion method and purified by differential adhesion method. The cardiomycoytes and their purity were identified by troponin and actin immunocytochemical staining

and ALD-induced cell injury models were established. The optimal ALD concentration and treatment duration were determined by 3-(4

5-dimethylthiazol-2-yl)-2

5-diphenyltetrazolium bromide (MTT) assay. The experiment was divided into 4 groups:blank group (serum free cell culture)

ALD group (optimal concentration)

OMT high dose group (ALD+100 mg·L-1 OMT) and OMT low dose group (ALD+50 mg·L-1 OMT). Preincubated with OMT 2 h

and then ALD was added for co-culture for 36 h. The protection effects of OMT on ALD-induced injury were detected and analyzed by MTT assay and lactate dehydrogenase (LDH) leakage assay. Reverse transcription PCR (RT-PCR) was used to analyze the mRNA of mineralocorticoid receptor (MR). The protein expression levels of MR and CYP11B2 were detected by Western blot. Result: The 16 mg·L-1 ALD significantly induced cell injury after 36 h. ALD-induced cardiomyocyte viability decrease and LDH leakage increase were significantly attenuated by OMT (100

50 mg·L-1). Furthermore

OMT (100

50 mg·L-1) suppressed ALD-induced up-regulation of MR mRNA levels and protein expression levels

and enhanced protein expression of CYP11B2. Conclusion: OMT had protection effects on ALD-induced cardiomyocyte injury

and the mechanism may be associated with inhibiting ALD/MR signaling activation.