Calenduloside E Ameliorates Myocardial Ischemia-Reperfusion Injury through Regulation of AMPK and Mitochondrial OPA1

Figure 6

Effects of OPA1 on the protection of CE against H/R-stimulated mitochondrial injury and apoptosis. The siRNA against OPA1 was used to knock down the expression of OPA1. (a) Western blot assay and quantitative analyses of mitochondrial fission-related (Drp1 and Fis1) and fusion-related (OPA1 and Mfn2) proteins in H/R cardiomyocytes with CE and OPA1 siRNA pretreatment. (b) Effects of CE and OPA1 deficiency on cell viability in H/R-treated cardiomyocytes. (c) Effects of CE and OPA1 deficiency on ATP levels. (d) Effects of CE and OPA1 deficiency on mitochondrial transmembrane potential based on JC-1 staining. (e) Quantitative analysis of mitochondrial membrane potential. (f) Effects of CE and OPA1 deficiency on apoptotic proteins cleaved caspase-3 and cleaved PARP. β-Actin expression was examined as a protein loading control. Data are presented as the from three independent experiments. ^## vs. control; vs. H/R; vs. H/R; ^& vs. H/R+CE; ^&& vs. H/R+CE.

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