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. 2020 Sep;8(17):1064. doi: 10.21037/atm-20-2118

Figure 5.

Figure 5

CRP increases cardiac function and ameliorates cardiac hypertrophy via PPARγ. (A) PPARγ inhibitor (1 mg/kg/d) abolished the prevention of CRP on Ang II-induced cardiac dysfunction evidenced by echocardiography for mice including decrease of ejection fraction (EF) and fractional shortening (FS) (n=8, 6, 6, 6); (B) Histological analysis with haematoxylin and eosin (H&E) staining revealed that PPARγ inhibitor (1 mg/kg/d) blocked the CRP-mediated inhibition of Ang II-induced pathological hypertrophy proved by enlargement of cell size in mice, scale bars =100 µm (n=8, 6, 6, 6); (C) qRT-PCR results showed that PPARγ inhibitor (1 mg/kg/d) blocked the prevention of CRP on Ang II-induced pathological hypertrophy evidenced by upregulation of hypertrophic markers (Anp and Bnp) expression in mice (n=8, 6, 6, 6). Data are presented as mean ± SD. *, P<0.05; **, P<0.01.CRP, Citri reticulatae Pericarpium; Ang II, angiotensin II; NRCMs, neonatal rat cardiomyocytes; Anp, natriuretic peptide type A; Bnp, natriuretic peptide B; PPARγ, peroxisome proliferator-activated receptor gamma.