中国当代医药2025，Vol.32Issue(6)：10-15,6.DOI:10.3969/j.issn.1674-4721.2025.06.02
褪黑素介导腺苷酸活化蛋白激酶抑制线粒体损伤降低大鼠心肌缺血再灌注损伤的机制
Mechanism of melatonin mediated adenylate activated protein kinase in-hibition of mitochondrial injury and reduction of myocardial ischemia-reperfusion injury in rats
摘要
Abstract
Objective To explore the protective mechanism of melatonin(Mel)mediated adenosine 5'-monophosphate-ac-tivated protein kinase(AMPK)pathway against myocardial ischemia/reperfusion injury(MI/RI).Methods A total of 50 SPF grade male SD rats were selected as research subjects,and they were randomly divided into 5 groups,with 10 rats in each group.In Sham operation group,the left anterior descending coronary artery was not ligated.In the Mel group,the left anterior descending coronary artery was not ligated,and a single intraperitoneal injection of melatonin was given.The vehicle(V)control group(MI/RI+V group)was established by coronary artery ligation,and ethanol-saline was injected intraperi-toneally before modeling and reperfusion.In the Mel treat-ment group(MI/RI+Mel group),melatonin was injected intraperitoneally before modeling and reperfusion.In MI/RI+Mel+BML275 group,BML275 was intraperitoneally injected before modeling and reperfusion,and melatonin was in-traperitoneally injected before reperfusion.A MI/RI model was established by coronary artery ligation,and the pathological results were observed by hematoxylin-eosin(HE)staining.The cardiac function and serum levels of troponin T(TnT),lactate dehydrogenase(LDH),and creatine kinase(CK)were detected in rats.Evans blue-triphenyltetrazolium chloride(TTC)dou-ble staining method was used to observe myocardial infarction.Western blot was used to detect the expression of adenosine 5'-monophosphate-activated protein kinase(AMPK α),dynamin-related protein 1(Drp1),and cytochrome C(Cyt C)in my-ocardial tissue.Results The left ventricular ejection fraction(LVEF)and left ventricular shortening fraction(LVFS)of the MI/RI+Mel group and the MI/RI+Mel+BML275 group were higher than those of the MI/RI+V group,while the LVEF and LVFS of the MI/RI+Mel+BML275 group were lower than those of the MI/RI+Mel group,with statistically significant differences(P＜0.05).The serum TnT,CK,and LDH levels in the MI/RI+Mel group and MI/RI+Mel+BML275 group were lower than those in the MI/RI+V group,while the serum TnT,CK,and LDH levels in the MI/RI+Mel+BML275 group were higher than those in the MI/RI+Mel group,with statistically significant differences(P＜0.05).The myocardial infarction area in the MI/RI+Mel group and MI/RI+Mel+BML275 group were smaller than that in the MI/RI+V group,while the myocardial infarction area in the MI/RI+Mel+BML275 group was larger than that in the MI/RI+Mel group,with statistically significant differences(P＜0.05).The expression of phosphorylation adenosine 5'-monophosphate-activated protein kinase α(p-AMPKα)in the MI/RI+Mel group and the MI/RI+Mel+BML275 group were higher than that in the MI/RI+V group,while the expression of p-AMPKα in the MI/RI+Mel+BML275 group was lower than that in the MI/RI+Mel group,with statistically significant differences(P＜0.05).The expression of phosphorylation dynamin-related protein 1(p-Drp1)/Drp1 and Cyt C in the MI/RI+Mel group and MI/RI+Mel+BML275 group were lower than that in the MI/RI+V group,and the expression of p-Drp1/Drp1 and Cyt C in the MI/RI+Mel+BML275 group were higher than that in the MI/RI+Mel group,and the differences were statistically significant(P＜0.05).Conclusion Mel can inhibit mitochondrial damage by activating AMPK pathway,reduce MI/RI injury,and improve cardiac function.关键词
褪黑素/心肌缺血/再灌注损伤/大鼠/腺苷酸活化蛋白激酶通路/线粒体损伤Key words
Melatonin/Myocardial ischemia/reperfusion injury/Adenosine 5'-monophosphate-activated protein kinase pathway/Mitochondrial damage分类
医药卫生引用本文复制引用
曾明辉,余龙辉,邱明涛,李晨..褪黑素介导腺苷酸活化蛋白激酶抑制线粒体损伤降低大鼠心肌缺血再灌注损伤的机制[J].中国当代医药,2025,32(6):10-15,6.基金项目
江西省卫生健康委科技计划项目(202410765). （202410765）
