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Western blot results cardiomyocytes8/11/2023 ![]() Zanger UM, Schwab M (2013) Cytochrome P450 enzymes in drug metabolism: regulation of gene expression, enzyme activities, and impact of genetic variation. Manikandan P, Nagini S (2018) Cytochrome P450 structure, function and clinical significance: a review. Williams LJ, Nye BG, Wende AR (2017) Diabetes-related cardiac dysfunction. Lorenzo-Almoros A, Tunon J, Orejas M, Cortes M, Egido J, Lorenzo O (2017) Diagnostic approaches for diabetic cardiomyopathy. Katz AM, Freston JW, Messineo FC, Herbette LG (1985) Membrane damage and the pathogenesis of cardiomyopathies. McKenna WJ, Maron BJ, Thiene G (2017) Classification, epidemiology, and global burden of cardiomyopathies. These findings suggested that Cyp2e1 might be potentially used as an effective therapeutic strategy for DCM. ConclusionsĬyp2e1 knockdown attenuated HG-induced apoptosis and oxidative stress by activating PI3K/Akt signaling in cardiomyocytes. Inhibition of PI3K/Akt using LY294002 reversed the inhibitory effects of Cyp2e1 knockdown on cell apoptosis and ROS generation on cardiomyocytes. Increased relative levels of p-PI3K/PI3K and p-Akt/Akt were found in Cyp2e1-knockdown H9c2 and HL-1 cells. Cyp2e1 knockdown reduced ROS generation and elevated the expression level of nuclear Nrf2 in HG-induced H9c2 and HL-1 cells. Cyp2e1 knockdown attenuated HG-induced apoptosis in both H9c2 and HL-1 cells, as proved by deceased apoptotic rate, relative cleaved caspase-3/caspase-3 level, and caspase-3 activity. In vitro assays proved that Cyp2e1 expression was markedly increased in HG-induced H9c2 and HL-1 cells. Resultsįrom the bioinformatics analysis, Cyp2e1 was confirmed as an upregulated gene in DCM tissues. Reactive oxygen species (ROS) generation was examined by DCFH2-DA staining assay. TUNEL assay was performed to assess apoptotic rate. Western blot analysis was performed to determine the expression levels of Cyp2e1, apoptosis-related proteins and PI3K/Akt signaling-associated proteins. The Cyp2e1-knockdown H9c2 and HL-1 cells were established through transfection with si-Cyp2e1. Identification of differentially expressed genes in DCM and control rats was performed using bioinformatics analysis based on GEO database. Thus, we intended to identify the effects of Cyp2e1 on cardiomyocytes under high glucose (HG) conditions. However, the role of Cyp2e1 in diabetic cardiomyopathy (DCM) has never been reported. Myocardial ischaemia/reperfusion injury YAP1 cardiomyocytes apoptosis lncRNA CRNDE.Cyp2e1 is a crucial CYP450 enzyme participating in diabetes and cardiovascular disorder. Our study suggested that lncRNA CRNDE could regulate YAP1 level by ubiquitination and proteasomal degradation pathway, thus inhibiting cardiomyocytes apoptosis in MI/R injury. After transfection of Si-YAP1 in the H/R-treated HL-1 cells transfected with pc-DNA CRNDE, the protein level of Bcl-2 was decreased, while cleaved caspase-3 expression and the apoptosis rate were increased. Furthermore, lncRNA CRNDE could bind to YAP1 and regulated the protein level of YAP1 by ubiquitination and proteasomal degradation pathway. ![]() The expressions of YAP1 and Bcl-2 were decreased, while the expression of cleaved caspase-3 was increased after the knockdown of lncRNA CRNDE. The extent of cardiomyocytes apoptosis was significantly increased, and the levels of lncRNA CRNDE, YAP1 and Bcl-2 were down-regulated, while cleaved caspase-3 expression was up-regulated in MI/R mice and H/R-treated HL-1 cells. RIP assay was used to detect the interaction between lncRNA CRNDE and YAP1. Flow cytometry was used to determine the apoptosis rate of cardiomyocytes. The protein expressions of YAP1, Bcl-2 and cleaved caspase-3 were detected by western blot analysis. QRT-PCR was used to validate lncRNA CRNDE level in myocardial tissues and HL-1 cells. Apoptotic levels were assessed by TUNEL staining assay. MI/R model in vivo and hypoxia/re-oxygenation (H/R) model in vitro were constructed. The aim of this study is to explore the specific effect of lncRNA CRNDE on cardiomyocytes apoptosis. Long non-coding RNA colorectal neoplasia differentially expressed (lncRNA CRNDE) can inhibit cell apoptosis, but its specific role in MI/R injury has not been studied. Cardiomyocytes apoptosis is the basic pathological process of myocardial ischaemia/reperfusion (MI/R) injury, so inhibiting apoptosis of cardiomyocytes can effectively improve MI/R injury. ![]()
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