Protection of crocetin on myocardial ischemia-reperfusion injury in rats / 中草药

ABSTRACT

Objective To study the protection of crocetin on myocardial ischemia-reperfusion injury and the possible mechanism involved. Methods Infarction model Coronary occlusion was maintained for 45 min and reperfused for 180 min to produce infarction model. Creatine kinase (CK) and lactate dehydrogenase (LDH) activity in serum of infarction groups were analyzed at baseline (before ischemia), 5, 60, and 180 min after reperfusion. Stunned model Stunned model was achieved by ligating the left anterior descending branch of coranary artery for 15 min. Na+, K+-ATPase, and Ca2+, Mg2+-ATPase activity, total adenosine content (TAC), and energy charge (EC) in ischemic and nonischaemic myocardial tissue and malondialdehyde (MDA) in serum of stunned groups were analyzed at the end of 180 min of reperfusion. Haemodynamic parameters including heart rate, left ventricular end-systolic and end-diastolic pressure, ejection fraction, maximum and minimum dp/dt, maximum and minimum dV/dt, and stroke work, were monitored at baseline, 5, 30, 90, and 180 min after reperfusion. Results Crocetin could attenuate the infarction ratio, relieve stunning in a dose-dependent manner, and decrease the CK and LDH activities in serum. Crocetin (50 mg/kg) could improve the heart function, ameliorate myocardial stunning degree, and increase the level of ATP and EC in myocardial tissue. Conclusion Crocetin could protect myocardium from ischemia and following reperfusion, then prevent the myocardial infarction and relieve myocardial stunning. The underlying mechanism may be partly attributed to the improvement of energy restoration and free radical scavenging effect.