Objective: To discuss the protective effect and potential mechanism of ginsenosides CK on rat's myocardial ischemia reperfusion injury (MIRI). Method: SD rats were randomly divided into 5 groups:sham-operated group

MIRI group (normal saline) and ginsenosides CK low

medium and high-dose groups (10

20

40 mg·kg-1). Ginsenosides CK was intraperitoneally injected for 14 days. the anterior descending coronary artery was ligated; 30 min later

reperfusion was performed for 120 min to establish the reperfusion model. Effects of ginsenosides CK on infarct area

levels of serum lactic denydrogenase(LDH)

creatine phosphokinase(CPK)

inducible nitric oxide synthase(iNOS)

interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α)

and malondialdehyde(MDA) content

super oxide dismutase(SOD) activity and high mobility group box-1(HMBG1) expression were investigated. Result: Compared with the normal group

the MIRI group showed significant increase in MDA content in myocardia

serum iNOS

IL-6 and TNF-α levels

and HMGB1 protein in myocardia

and significant decrease in SOD activity (P<0.05). Ginsenosides CK could reduce the infarct size and activities of LDH and CPK compared with those in the MIRI group (P<0.05). Ginsenosides CK could lessen the MDA contents and SOD activity of cardiac muscle tissues compared with those in the MIRI group (P<0.05). Ginsenosides CK could lower the levels of iNOS

IL-6 and TNF-α compared with those in the MIRI group (P<0.05). Meanwhile

Ginsenosides CK could inhibit the expression of HMBG1 compared with those in the MIRI group (P<0.05). Conclusion: Ginsenosides CK has a certain protective effect on myocardial ischemia-reperfusion injury in rats

and its effect is related to the enhancement in antioxidant capacity

the reduction of inflammation and the inhibition of the HMBG1 expression.