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目的：：研究11-羰基-β-乙酰乳香酸( AKBA)对盐酸异丙肾上腺素( ISO)诱导大鼠心肌缺血损伤的保护作用机制。方法：SD大鼠随机分为空白组、模型组、AKBA低剂量组、AKBA高剂量组。皮下注射ISO 100 mg·kg-1诱导心肌缺血损伤模型后,测定各组大鼠心电图ST段变化,检测血清的肌酸激酶同工酶( CK-MB)、心肌钙蛋白I( cTnI)、乳酸脱氢酶( LDH)、丙二醛( MDA)、超氧化物歧化酶( SOD)的含量变化,观察心肌组织病理性改变,检测心肌细胞的凋亡情况。结果：AKBA高剂量组大鼠心电图ST段移位显著低于模型组；AKBA高剂量组能显著降低大鼠血清中心肌酶的CK-MB、cTnI、LDH；AKBA高剂量组降低大鼠血清中MDA,升高SOD活力；AKBA高剂量组的心肌组织病理损伤小于模型组；AKBA高剂量组抑制心肌缺血损伤中的心肌细胞的凋亡。结论：AKBA组能有效抑制ISO所致心肌缺血损伤,抑制心肌细胞凋亡,对心肌具有保护作用。“,”Objective:To study the effects and mechanisms of acetyl-11-keto-β-boswellic acid ( AKBA) in myocardial ischemic model induced by isoproterenol hydrochloride ( ISO) in rats. Methods:The SD rats were randomly divided into the sham group, model group, AKBA low dose group and AKBA high dose group. Myocardial injury model was induced by subcutaneous injection of ISO (100 mg·kg-1 ) . The change of ST segment in ECG was observed. Creatine kinase ( CK-MB) , cardiac troponin I ( cTnI) , lactate dehydro-genase( LDH) , malondialdehyde( MDA) and superoxide dismutase( SOD) in the blood were detected by ELISA. The change of histo-logical tissue was determined by HE staining, and cell apoptosis was analyzed by TUNEL assay. Results: Serum CK-MB, cTnI and LDH were decreased significantly in AKBA high dose group when compared with those in the model group. Compared with that in the model group, MDA content was lowered and the SOD activity was increased in AKBA high dose group. Furthermore, AKBA high dose group improved the pathologic changes of myocardium. TUNEL assay revealed significant reduction of cardiomyocytes apoptosis in the hearts of the ischemic rats in AKBA high dose group. Conclusion:AKBA has excellent cardioprotective effect on myocardial ischemic induced by ISO and protection of myocardial cells from injury.