Research Article
circ_0023461 Silencing Protects Cardiomyocytes from Hypoxia-Induced Dysfunction through Targeting miR-370-3p/PDE4D Signaling
Figure 6
miR-370-3p overexpression-mediated protective effects in hypoxia-induced cardiomyocytes are partly counteracted by the introduction of PDE4D plasmid. (a) The transfection efficiency of PDE4D plasmid in AC16 cells was assessed by Western blot assay. (b–l) AC16 cells were divided into the following four groups: hypoxia+miR-NC, hypoxia+miR-370-3p, hypoxia+miR-370-3p+vector, and hypoxia+miR-370-3p+PDE4D. (b) CCK8 assay was conducted to assess cell viability. (c) Edu assay was performed to analyze the proliferation ability of AC16 cells. (d) Cell migration ability was assessed by Transwell migration assay. (e) The apoptosis of AC16 cells was analyzed by flow cytometry. (f, g) Cell oxidative status was analyzed using the matched kits. (h) The release of IL-6 and TNF-α was analyzed by ELISA. (i–k) The uptake of glucose and the production of lactate and ATP were analyzed using their matched colorimetric assay kits. (l) The expression of HK2 and LDHA was analyzed by Western blot assay. .
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