利拉鲁肽对大鼠心肌缺血再灌注损伤的作用分析-effect of liraglutide on myocardial ischemia-reperfusion injury in rats.docxVIP
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利拉鲁肽对大鼠心肌缺血再灌注损伤的作用分析-effect of liraglutide on myocardial ischemia-reperfusion injury in rats
利拉鲁肽对大鼠心肌缺血再灌注损伤的作用研究摘要目的:研究利拉鲁肽对大鼠心肌缺血再灌注损伤的作用,进一步探讨其可能介导的机制。方法:SD大鼠48只,雄性,随机数字表法分为假手术组、缺血再灌注组(I/R组)和利拉鲁肽组。通过结扎左冠状动脉前降支(LAD)30min再灌注2h建立大鼠心肌缺血再灌注损伤的实验模型。苏木素伊红染色法光镜下观察大鼠心肌组织的病理形态学改变;2,3,5-三苯基氯化四氮唑染色法测定各组大鼠心肌梗死面积;免疫组织化学法测定心肌组织中半胱氨酸天冬氨酸蛋白酶-3(caspase-3)和P53的表达;黄嘌呤氧化酶法检测血清超氧化物歧化酶(SOD)活性,硫代巴比妥酸法测定丙二醛(MDA)浓度。结果:苏木素伊红染色结果示利拉鲁肽组大鼠心肌损伤程度明显较I/R组轻。与I/R组相比,利拉鲁肽组大鼠的心肌梗死面积较小[(0.44±0.08)%比(0.62±0.08)%,P0.05)],caspase-3表达水平较低(0.19±0.03比0.24±0.02,P0.05),p53的表达水平较低(0.27±0.03比0.39±0.04,P0.05),血清SOD活性较高(74.20±11.10比44.04±14.30,P0.05),MDA浓度较低(4.41±1.07比8.72±2.20,P0.05)。结论:利拉鲁肽可对抗大鼠心肌缺血再灌注损伤,对心肌具有保护作用,其机制可能由抗细胞凋亡和抗氧化应激作用介导。I关键词:心肌缺血再灌注损伤;心肌梗死面积;利拉鲁肽IIEffectofLiraglutideonmyocardialischemia/reperfusioninjuryinratsAbstractObjective:Tostudytheeffectofliraglutideonmyocardialischemia/reperfusion(I/R)injuryinratsanditspossiblemechanism.Methods:Forty-eightmaleSDratsweredividedintoshamgroup,I/Rinjurygroup,andliraglutidegroupbytableofrandomnumber.AratmyocardialI/Rinjurymodelwasestablishedbyocclusionoftheleftanteriordescendingartery30minutesfollowedby2.0hoursofreperfusion.HEstainmethodwasusedtoobservecardiomyocytebylightmicroscope;MyocardialtissuesampleswerestainedwithTTCtomeasurethemyocardialinfarctionsize;Expressionofp53andcaspase-3proteinwereanalysisedbyimmunohistochemicaltechnique;XanthineoxidasemethodwasusedtodetectSODactivityofeachgroup;ThiobarbituricacidmethodwasusedtoobservetheconcentrationofMDA.Results:ComparedwiththeI/Rgroup,(1)thedegreeofmyocardialdamageofliraglutidegroupislitter;(2)themyocardialinfarctareawassignificantlylower[(0.44±0.08)%vs.(0.62±0.08)%,P0.05];(3)expressionofcaspase-3andp53inliraglutidegroupwaslowerthanI/Rgroup[(0.19±0.03)vs.(0.24±0.02)and(0.27±0.03)vs.(0.39±0.04),P0.05];(4)SODactivityincreasedsignificantlyandMDAdecreasedinliraglutidegroup[(74.20±11.10)vs.(44.04±14.30)and(4.41±1.07)vs.(8.72±2.20),P0.05)].Conclusions:LiraglutideprotectsmyocardiumagainstI/Rinjury,possiblybypreventingmyocardialcellsfromapoptosisandoxidation.Keywords:Myocardialischemiareperfusioninjury;My
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