黄芩素对大鼠心肌缺血再灌注损伤心肌酶的影响

Objective：To investigate the protective effects of baicalein（Bai）on rat heart ischemia-reperfusion injury caused by coronary artery ligation. Methods: Rat heart IPR injury was induced by occluding the left anterior descending coronary artery for 30 minutes and restoring blood perfusion for 30 minutes. Three dosages (40 mg/kg，80 mg/kg，160 mg/kg，respectively ) of Bai were intravenously injected before heart ischemia . Plasma creatine kinase (CK ) , creatine kinase isoenzyme B (CK-MB) , lactate dehydrogenase (LDH) , α-Hydroxybutyrate dehydrogenase (HBDH) , grutamic oxalacetic transaminase(GOT), malondiadehyde (MDA) concentrations and superoxide dismutase(SOD) activity were measured. The pathologic changes of I/R injury were observed on the microscopy. Results:：Bai reduced the release of CK, CK-M B, LDH , HBDH and GOT from I/R rat hearts , increased the activity o f SOD and decreased the MDA product . In Bai (1 mgokg-1) group, the serum CK-MB, LDH and HBDH concentrations were lowered significantly ( vs I/R group P<0.05) . In Bai (40, 80, 160 mg/kg) significantly (vs I/R group P<0.05), and SOD activity increased significantly (vs I/R group P <0.05). The decrease groups, serum CK, CK-MB, LDH, HBDH and GOT concentrations and MDA content were decreased of CK, CK-MB, LDH, HBDH and MDA in Bai (80,160 mg/kg) group was more remarkable than that in Bai (40 mg/kg) group ( P<0.01) . CK-M B in Bai (40 mg/kg) group was lower than that in Verapamil (2 mg/kg) group (P<0.05). For morphology, myocytes of I/R heart showed intracellular edema, disarrangement and rapture of myocardial fiber, damaged mitochondria, marginated and concentrated nucleus. Bai mollified these changes. Conclusion: Bai may exert an apparent role against rat heart ischemia-reperfusion injury in dose-dependent manner.