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机构地区:[1]内蒙古医科大学基础医学院内蒙古自治区分子生物学重点实验室,呼和浩特010059 [2]中国医学科学院药物研究所,北京100050 [3]内蒙古医科大学附属医院,呼和浩特010059
出 处:《中南药学》2015年第2期147-150,共4页Central South Pharmacy
摘 要:目的研究蒙古黄芪总黄酮对大鼠心肌缺血再灌注损伤的保护作用及其机制。方法采用结扎大鼠左冠状动脉前降支法,缺血90 min,再灌注24 h,建立心肌缺血再灌注损伤模型。观察大鼠心电图S-T段变化,用氯化三苯基四氮唑(TTC)对心肌染色,观察心肌梗死面积及测定血清乳酸脱氢酶、肌酸激酶、心肌组织超氧化物歧化酶、丙二醛含量,探讨蒙古黄芪总黄酮对心肌缺血再灌注损伤的保护作用。结果蒙古黄芪总黄酮90、270 mg·kg-1可以使心肌缺血再灌注损伤大鼠心电图S-T段降低及降低大鼠血清中乳酸脱氢酶、肌酸激酶的释放;30、90、270 mg·kg-1剂量可减少大鼠心肌梗死面积;270 mg·kg-1剂量减少大鼠心肌组织丙二醛的产生,提高心肌组织超氧化物歧化酶活力。结论蒙古黄芪总黄酮可以使缺血再灌注损伤大鼠心肌缺血程度降低,减少心肌梗死面积,对缺血再灌注损伤具有一定的保护作用,其作用机制可能通过抑制乳酸脱氢酶、肌酸激酶的释放,降低心肌组织氧化产物丙二醛含量、提高内源性氧自由基清除剂超氧化物歧化酶的活力,减轻缺血再灌注损伤后氧自由基对心肌细胞膜脂质过氧化损伤有关。Objective To determine the protective effect and potential mechanism of total flavonoids from Astragalus Mongholicus(TFAM) on myocardial ischemia-reperfusion injury in rats. Methods The ischemia-reperfusion injury model was established by occluding the anterior descending of the left artery in rats, and opened for 24 h after occluding left anterior descending coronary artery(LAD) for 90 min. We observed the changes of the S-T segment of electrocardiogram andmyocardial infarct size by staining with TTC. The activity of lactate dehydrogenase, creatine kinase, levels of the superoxide dismutase, maleic dialdehyde in the serum and cardiac tissue were measured by reagent kit. Results TFAM(90 and 270 mg·kg^- 1) lowered the height the of S-T segment of electrocardiogram and obviously reduced the activity of CK and LDH. TFAM(30, 90 and 270 mg·kg^- 1) reduced the myocardial infarction size on ischemia-reperfusion injury model. TFAM(270 mg·kg^- 1) decreased the level of MDA and increased the content of SOD. Conclusion TFAM can reduce the degree of myocardial ischemia and myocardial infarction area. It has certain protective effects against myocardial ischemia-reperfusion injury in rats via attenuating oxygen free radical and inhibiting inflammatory reaction.
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