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

Figure 2

NOB mitigates pathological cardiac remodeling after MI. (a) Masson’s trichrome staining indicated that the fibrosis rate of the peri-infarct area descended significantly after NOB intervention (blue, fibrosis-positive area; red, fibrosis-negative area; scale bars: 50 μm) (, 8, 6, and 8). (b) Western blot analysis revealed that collagen I and α-SMA were dramatically decreased in NOB intervention mice after MI ( per group). (c) qRT-PCR analysis of collagen I and collagen III showed that NOB alleviated cardiac fibrosis after MI ( per group). (d) qRT-PCR analysis showed that NOB alleviated the upregulation of ANP and BNP induced by MI ( per group). (e) HE staining revealed that the cross-sectional areas of cardiomyocytes were smaller in the intervention group than in the MI group (scale bars: 50 μm, , 8, 6, and 8). WGA staining illuminated the same trends as HE staining: the increased cross-sectional areas of cardiomyocytes were smaller after NOB intervention (scale bars: 20 μm, per group). (f) Western blot showed that the ratio of Bax/Bcl2 and the expression of cleaved caspase-3 were both lower in the NOB intervention group than in the MI group ( per group for Bax/Bcl2 and per group for cleaved caspase-3). (g) TUNEL staining displayed that the upregulated apoptotic-positive cardiomyocyte rate was decreased after NOB intervention in cardiac tissue (blue: nuclei; green: apoptotic-positive nuclei; scale bars: 100 μm, per group). Data are presented as . ; ; ; ^ns. NOB: nobiletin; MI: myocardial infarction; ANP: natriuretic peptide type A; BNP: natriuretic peptide B; HE staining: haematoxylin and eosin staining; WGA staining: wheat germ agglutinin; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling.

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