Objective: To study the effect of leonurine on myocardial ischemia and myocardial cell injury caused by acute myocardial infarction

and its functional mechanism. Method: The model of acute myocardial infarction in rats was established through ligation of the left anterior descending coronary artery. Male SD rats were randomly divided into five groups:sham-operated group

leonurine high-dose (30 mg · kg-1 · d-1) group

low-dose (15 mg · kg-1 · d-1) group

positive control group and model group. One week before the coronary artery ligation

all groups

except for the sham-operated group

were given the corresponding dose of drugs. The model was built on the eighth day

and postoperative intraperitoneal administration lasted for 2 days. The animals were sacrificed

and myocardial infarct size was measured by TTC staining. The content of lactate dehydrogenase (LDH)

creatine kinase (CK)

superoxide dismutase (SOD) and malondialdehyde (MDA) in rat serum were determined with enzyme-linked immuno sorbent assay (ELISA) kit. Result: Compared with the sham-operated group

the model group showed significant increase in myocardial infarct size

and serum LDH

CK and MDA content

and significant decrease in total superoxide dismutase (T-SOD) (P<0.05

P<0.01); compared with the model group

the leonurine group showed significant decrease in myocardial infarct size

and serum LDH

CK and MDA content

and significant increase in total superoxide dismutase (T-SOD) (P<0.05

P<0.01). Conclusion: Leonurine has a good protective effect on myocardial injury caused by acute myocardial ischemia. Its mechanism may be related to the improvement of the antioxidant capacity of myocardial tissues.