【摘要】 目的:观察硫化氢（hydrogen sulfide,H₂S）对异丙肾上腺素（isoproterenol,ISO）诱导小鼠急性心肌损伤的保护作用及可能机制。方法:12周龄C57BL/6小鼠,腹腔注射H₂S供体硫氢化钠（Na HS）10μmol/（kg·d）2周,然后再联合给予大剂量ISO[150 mg/（kg·d）]皮下注射2 d,观察心肌组织病理结构,检测血浆肌酸激酶（creatine kinase,CK）、乳酸脱氢酶（lactate dehydrogenase,LDH）活性,评估心肌组织活性氧、丙二醛（malondialdehyde,MDA）、总抗氧化能力（total antioxidant capacity,T-AOC）及超氧化物岐化酶（superoxide dismutase,SOD）活性与表达。结果:Na HS预处理改善大剂量ISO诱导的小鼠心肌组织病理结构紊乱,降低血浆CK和LDH活性,降低心肌活性氧和MDA水平,提高心肌T-AOC,增强心肌SOD活性和表达。结论:H₂S减轻ISO诱导小鼠急性心肌损伤,机制可能与提高SOD表达与活力、减轻氧化应激有关。更多还原

【Abstract】 Objective:To observe the protective effects and mechanisms of hydrogen sulfide(H2 S)on isoproterenol(ISO)induced acute myocardial injury in mice. Methods:C57 BL/6 mice of 12-week-old were subcutaneously injected with H2 S donor Na HS[10 μmo L/(kg·d)]for 2 weeks,and then large dosage of ISO[150 mg/(kg·d)]was jointly given by subcutaneous injection for 2 days. Pathological structures of myocardium were assessed. Activities of creatine kinase(CK)and lactate dehydrogenase(LDH)in plasma were measured.Levels of reactive oxygen species(ROS)and malondialdehyde(MDA),total antioxidant capacity(T-AOC),activity and expression of superoxide dismutase(SOD)in myocardium were detected. Results:Na HS pretreatment improved ISO induced pathological disorder in the myocardium,reduced CK and LDH activity in the plasma,decreased the level of myocardial ROS and MDA,improved myocardial T-AOC,enhanced myocardial SOD activity and expression. Conclusion:H2 S alleviated ISO induced acute myocardial injury in mice,which might be associated with the improvement of SOD expression and activity,and the reduction of oxidative stress.更多还原