Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPARγ and PGC1α

Figure 3

NOB attenuates hypoxia-induced apoptosis and PE-induced cardiac hypertrophy in NRVMs. (a) Western blot analysis of Bax and Bcl2 indicated that the Bax/Bcl2 ratio increased after hypoxia and decreased with NOB administration ( per group). (b) TUNEL staining indicated that the rate of apoptosis-positive NRVMs was reduced after NOB interference compared with that in the hypoxia group (blue: nuclei; red: α-actinin; and green: apoptotic-positive nuclei; scale bars: 100 μm, per group). (c) Immunofluorescence staining in NRVMs (blue: nuclei; green: α-actinin; scale bars: 100 μm) showed that the NRVM cell size increased in the PE group compared with the control group, which could be reversed by NOB intervention ( per group). (d) qRT-PCR showed that the expression levels of ANP and BNP were lower in the NOB intervention group than in the PE-induced group ( per group). Data are presented as . ; ; ; ^ns. NOB: nobiletin; NRVMs: neonatal rat ventricular cardiomyocytes; PE: phenylephrine; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling; ANP: natriuretic peptide type A; BNP: natriuretic peptide B.

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