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. 2022 Jan 18;12:784041. doi: 10.3389/fphar.2021.784041

FIGURE 4.

FIGURE 4

Curcumin inhibits cardiac fibrosis by regulating macrophage-fibroblast crosstalk instead of directly suppressing cardiac fibroblast trans-differentiation (A). Fibrotic protein expression in different NRCF group (WT, WT + TGF-β, TGF-β+RAW (LPS), TGF-β+RAW (LPS + Cur)) respectively, fibrotic protein is defined as EDA-Fibronectin, periostin, vimentin and α-SMA (B). Fibrotic protein expression in different NRCF group (WT, WT + TGF-β, WT + TGF-β+Cur) respectively (C-F). Summary data of protein expression are displayed in (A), EDA-fibronectin are plotted in (C), periostin is plotted in (D), vimentin is plotted in (E) and α-SMA is plotted in (F) (G–J). Summary data of protein expression displayed in (B), EDA-Fibronectin was plotted in (G), periostin was plotted in (H), vimentin is plotted in (I) and α-SMA in J) (K–M). TGF-βR1 downs-stream signaling identification by western blot in each group (WT, WT + TGF-β, TGF-β+RAW (LPS), TGF-β+RAW (LPS + Cur)); phosphorylated SMAD2 and SMAD3 were determined as key factors underlying TGF-βR1 signaling to promote fibrosis procedure. Western blot bands are displayed in (K), and summarized data are plotted in (L-M) (N-P) Phosphorylation level of SMAD2/3 in respective groups (Sham, MI, MI + Cur 50 mg/kg, MI + Cur 100 mg/kg) 1 month after MI were detected by western blotting, bands are shown in (N), and summarized data are plotted in (O–P). Results are mean with SEM, NS = no significance between groups, *p < 0.05, **p < 0.01.