Objective: To explore the effect and mechanism of Ziziphora clinopodioides flavonids (ZCF) on oxygen free radicals

nitric oxide(NO) and cell apoptosis of myocardial ischemia-reperfusion injury (MIRI) in rats. Method: Totally 60 rats were randomly divided into sham group

MIRI model group

compound Danshen dripping pills group (130 mg·kg-1)

low

medium and high-dose ZCF groups (75

150

300 mg·kg-1). The model of MIRI was established by ligating the left anterior descending coronary artery (LAD) for 30 min

which was followed by a 3 h reperfusion. The levels of creatine kinase isozyme (CK-MB)

lactate dehydrogenase (LDH)

superoxide dismutase (SOD)

glutathione peroxidase (GSH-Px)

malondialdehyde (MDA)

nitric oxide (NO) and nitric oxide synthase (NOS) in serum were measured. The degree of myocardial infarction was evaluated by triphenyltetrazolium chlorid (TTC) staining

the pathological changes of myocardium in rats were observed by hematoxylin and eosin (HE) staining

and the cell apoptosis was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL). Quantitative Real-time PCR was utilized to measure Bcl-2 and Bax mRNA expressions. Result: Compared with the shame group

the content of CK-MB

LDH

MDA showed significant increases

while the activities of SOD

GSH-Px

NO and NOS showed significant decreases in the model group. It also showed severe myocardial infarction and obvious cell apoptosis. The expression of Bcl-2 mRNA was significantly down-regulated

and the expression of Bax mRNA was significantly up-regulated (P<0.01). Compared with the model group

ZCF significantly decreased the content of CK-MB

LDH

MDA

and increased the activities of SOD

GSH-Px

NO and NOS. At the same time

the area of myocardial infarction was reduced

the pathological changes of ischemic myocardium were alleviated

and the cell apoptosis of myocardium was inhibited. The expression of Bcl-2 was significantly up-regulated

whereas the Bax mRNA expression was significantly down-regulated. The ratio of Bcl-2/Bax was significantly increased (P<0.05

P<0.01). Conclusion: ZCF can reduce the damage of ischemic myocardium in rats and play a role in protecting the myocardium. This may be related to the reduction of oxygen free radicals

the promotion of NO synthesis

the up-regulation of Bcl-2 and the down-regulation of Bax mRNA expression and the inhibition of the occurrence of myocardial cell apoptosis.