Wang, ZiliangZhang, HaoLiu, ZuhengMa, ZhuangAn, DongqiXu, Dingli2020-11-182020-11-182020-06Wang Ziliang, Zhang Hao, Liu Zuheng, Ma Zhuang, An Dongqi, Xu Dingli. Apigenin attenuates myocardial infarction-induced cardiomyocyte injury by modulating Parkin-mediated mitochondrial autophagy. Journal of Biosciences. 2020 Jun; : 1-90250-59910973-7138http://imsear.searo.who.int/handle/123456789/214286We aimed to detect whether the effect of apigenin (Apig) on the myocardial infarction-induced cardiomyocyte injury ofmouse myocardial cells and acute myocardial infarction (AMI) mice was through regulating Parkin expression viamiR-103-1-5p. The myocardial infarction cardiomyocyte model (Hypoxia/reoxygenation) was first constructed, thenthe mouse myocardial cells were treated with Apig, and the expression of miR-103-1-5p was decreased and theexpression of Parkin was increased by qRT-PCR and Western blot. It was confirmed by miRNA pulldown andluciferase reporter system that miR-103-1-5p in mouse myocardial cells can bind to Parkin mRNA and inhibit Parkinexpression. Next, a lentiviral vector silenced Parkin and overexpressing miR-103-1-5p was constructed and transfectedinto Apig-treated cells. Autophagy was detected by mitochondrial autophagy marker proteins [atypical protein kinaseC (aPKC)-interacting protein (p62) and bcl-2/Adenovirus E1B 19-kd interacting protein 3 (BNIP3)] via Western blot,mitochondrial function was detected by JC-1 probe, and apoptosis was detected by flow cytometry. It was confirmedthat Apig regulated mitochondria autophagy through miR-103-1-5p and Parkin, which ultimately affected cardiomyocyte death. Finally, an AMI mouse model was constructed, and then the mice were treated with Apig. Theinfarct size was detected by triphenyl tetrazolium chloride (TTC) staining, and the Apig relieved the myocardialinfarction. The expression of miR-103-1-5p was decreased and the expression of Parkin was increased by qRT-PCRand Western blot. The above results simplified that the cardio protection of Apig and miR-103-1-5p against injury ofmyocardial infarction cardiomyocyte by targeting Parkin. These results provided a novel treatment against myocardialinfarction cardiomyocyte.Apigenincardiomyocyte injurymicroRNA-103-1-5pmitochondrial autophagymyocardial infarctionParkinJournal ArticleIndiaState Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, ChinaDepartment of Cardiology, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, ChinaKey Laboratory for Organ Failure Research, Ministry of Education of the People’s Republic of China, Guangzhou 510515, ChinaState Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, ChinaKey Laboratory for Organ Failure Research, Ministry of Education of the People’s Republic of China, Guangzhou 510515, ChinaState Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, ChinaKey Laboratory for Organ Failure Research, Ministry of Education of the People’s Republic of China, Guangzhou 510515, ChinaState Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, ChinaKey Laboratory for Organ Failure Research, Ministry of Education of the People’s Republic of China, Guangzhou 510515, China