Apigenin attenuates myocardial infarction-induced cardiomyocyte injury by modulating Parkin-mediated mitochondrial autophagy

We 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.

Study on the Anti-apoptotic Effect of Curcumin on H 2O2-induced H 9c2 Cardiomyocyte Injury and the Regulation of NF-κB Signaling Pathway / 中国药房

OBJECTIVE：To investigate the anti-apoptotic effect of curcumin on H 2O2-induced H 9c2 cardiomyocyte injury and the regulation of NF-κB signaling pathway. METHODS：H9c2 cardiomyocyte were randomly divided into normal control group ， injury model group ，curcumin low-dose ，medium-dose and high-dose groups （25，50，100 μmol/L）. Normal control group didn ’t received any intervention. The cells in injury model group were induced with 50 μmol/L H2O2 for 12 h to establish the injury model. The cells in curcumin groups were treated with relevant concentration of drugs for 24 h，and then induced with 50 μmol/L H2O2 for 12 h. After cultured for 24 h，survival rate and apoptotic rate of cells were measured by MTT method and TUNEL method ；SOD activity and MDA content were determined by WTS- 8 assay and color test ；relative fluorescence intensity of LC 3 positive expression was detected by immunofluorescence method ；mRNA expression of NF-κB p65 in cells was detected by real-time PCR ； Western blotting assay was used to detect the protein expression of NF-κB p65 and p-NF-κB p65 in cells. RESULTS ：Compared with normal control group ，survival rate and SOD activity were decreased significantly in injury model group ，while apoptotic rate ， MDA content ，relative fluorescence intensity of LC 3 positive expression ，mRNA expression of NF-κB，protein expression of NF-κ B p 65 and p-NF-κB p65 as well as p-NF-κB/NF-κB were increased significantly（P＜0.05）. Compared with injury model group ， survival rates and SOD activities were increased significantly in curcumin groups ，while apoptotic rates ，MDA contents ，relative fluorescence intensities of LC 3 positive expression ，mRNA expression of LC 3 positive cells ，protein expression of NF-κB p65 and p-NF-κ B p65 as well as p-NF-κ B p65/NF-κ B p65 were decreased significantly （P＜0.05）. CONCLUSIONS ：Curcumin can increase the survival rate of H 2O2-induced H 9c2 cardiomyocyte injury ，decrease its apoptotic rate ，increase SOD activity and decrease MDA content in cardiomyocytes. Above effects may be related to the regulation of NF-κB signaling pathway.

Protective Effects of Quercetin on Daunorubicin-Induced Cardiomyocyte Injury / 实用儿科临床杂志

Objective To investigate the protective effects of quercetin on primary cultured SD neonate rats cardiomyocyte injury induced by daunorubicin.Methods Cultured cardiomyocytes were divided into blank groups,DNR groups,DNR+QUE groups,QUE groups.After preincubation of cardiomyocytes for 24 hours,cytoprotection effect was assessed by cell morphous,and cell apoptotic rates determined by flow cytometry,extracellular lactate dehydrogenase(LDH),superoxide dismutase(SOD) and malondialdehyde(MDA).Results Compared with DNR groups,the shedded cardiomyocytes and the cell debris of DNR+QUE groups decreased;the cardiomyocyte apoptosis rates decreased;the content of LDH and MDA decreased(P