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作 者:杨煜[1] 闻宇[2] 王友联 吕文伟[1] 康劲松[1] 李洪岩[1] YANG Yu;WEN Yu;WANG You-liang(Basic Medical College,Jilin University,Changchun 130021,China;Jilin University Second Hospital,Changchun 130041,China)
机构地区:[1]吉林大学基础医学院,吉林长春130021 [2]吉林大学第二医院,吉林长春130041
出 处:《中国实验诊断学》2022年第2期258-260,共3页Chinese Journal of Laboratory Diagnosis
基 金:吉林省卫生厅资助项目(2020J034)
摘 要:目的观察竹节参总皂苷对大鼠心肌缺血再灌注损伤的影响及机制。方法将雄性Wistar大鼠随机分为5组:假手术组、模型组、地奥心血康组50.0mg·kg^(-1)、竹节参总皂苷50.0mg·kg^(-1)组及100.0mg·kg^(-1)组。结扎大鼠心脏冠状动脉左前降支(LDA)30min再灌注120min,制备心肌缺血再灌注损伤模型,取血及心肌组织。利用生物试剂盒检测血清中天门冬酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的含量。流式细胞仪检测心肌细胞凋亡指数。透射电子显微镜下观察心肌细胞超微结构变化。结果与模型组比较,竹节参总皂苷可降低血清LDH、AST和MDA的含量及细胞凋亡指数,同时增加SOD和GSH-Px的含量,减轻缺血再灌注损伤对心肌细胞超微结构的损伤程度。结论竹节参总皂苷具有保护心肌缺血再灌注引起的心肌细胞损伤作用,其作用机制可能与清除氧自由基,降低脂质过氧化,减少心肌细胞凋亡有关。Objective To observe the effect and mechanism of total saponins of P.japonicus(TSPJ)on myocardial ischemia-reperfusion injury in rats.Methods Male Wistar rats were randomly divided into 5groups:sham operation group,model group,diao xinxuekang group(50.0 mg·kg^(-1)),TSPJ 50.0 mg·kg^(-1)group and 100.0 mg·kg^(-1)group.The myocardial ischemia-reperfusion injury model was made by ligation of the left anterior descending branch(LDA)of the rat’s heart coronary artery for 30min,and reperfusion for 120min,then the blood and myocardial tissue were prepared.The contents of aspartate aminotransferase(AST),lactate dehydrogenase(LDH),malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione peroxidase(GSH-PX)in serum were detected by biological kit.The apoptosis index of myocardial cells was detected by flow cytometry.The ultrastructural changes of myocardial cells were observed under transmission electron microscope.Results Compared with the model group,TSPJ could reduce the content of LDH,AST and MDA in serum and the apoptosis index,at the same time it could increase the content of SOD and GSH-PX,and reduce the damage degree of ischemia-reperfusion injury to the ultrastructure of myocadial cells.Conclusion TSPJ have the effect of protecting myocardial cells injury caused by myocardial ischemia and reperfusion,and its mechanism may be related to scavenging oxygen free radicals,reducing lipid peroxidation and reducing myocardial apoptosis.
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