Fig 2: Hearts of mice in the 32G TAC group had more fibrosis markers compared with those in the sham and 30G TAC groups. (A–C) Representative Masson staining of hearts of mice in the sham (A), 30G TAC (B), and 32G TAC (C) groups. The middle images are high-power fields of the corresponding left images (black square frame), showing interstitial fibrosis. The right images are high-power fields of the corresponding left images, showing perivascular fibrosis (green square frame, up) and endomyocardial fibrosis (blue square frame, down). Scale bar: 100 μm (left images); scale bar: 50 μm (middle and right images). (D) Interstitial fibrosis in the three groups; n = 3 hearts per group. Each heart slide was random selected with five high-power fields for statistical analysis. (E,F) qRT-PCR for the expression of Fn1 and Timp1 in the ventricular tissue; n = 6, sham; n = 6, 30G TAC; n = 6, 32G TAC. (G) Western blot stripes from three independent hearts in the three groups are shown. (H–L) Quantification of protein expression of TGF-β/β-tubulin (H), p-Smad3/Smad3 (I), MMP-9/β-tubulin (J), COL1A1/β-tubulin (K), and COL3/β-tubulin (L) in the hearts of mice in the sham, 30G TAC, and 32G TAC groups 14 days after the surgery. Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. Statistical significance was calculated using the unpaired two-tailed t-test.

Fig 3: Hypothetical scheme of the signal pathways mediating TGFB1-induced suppression of angiogenesis during follicular-luteal transition in vitro. TGFB1 binds to receptors leading to activation of ERK1/2 and PI3K/Akt signaling pathways and inhibition of ErbB signaling pathway. This suppresses the transcription of CLDN1, CDH1 and ESAM resulting in disruption of the cell adhesion junction, while increasing the expression of SDC1 and COL1A1 that inhibit ECM degradation, and promote the deposition of COL1A1. CLDN1, claudin 1; CDH1, E-cadherin; ESAM, endothelial cell-specific adhesion molecule; SDC1, syndecan-1; COL1A1, collagen type I alpha 1 chain; ECM, extracellular matrix.

Fig 4: Effect of TGFB1 on the expression of COL1A1, MMP3, SDC1 and CDH1 in bovine luteinizing follicular cells in vitro. Bovine luteinizing follicular cells (including granulosa, theca and endothelial cells) were treated with control or 10 ng/ml TGFB1 for 24 h and the mRNA expressions of COL1A1 and MMP3 were analyzed (A), Protein levels of COL1A1, SDC1, and CDH1 were examined using real-time qPCR (B) and western blot analysis (C), respectively.

Fig 5: Effects of C. sinensis extract pretreatment (25 and 50 μg/mL) for 4 h on the regulation of (A) mRNA expression of type 1 collagen (COL1A1) and elastin (ELN) and (B) mRNA expression of MMP9 and MMP1; protein levels of COL1A1 (C), ELN (D), MMP1 (E), and MPP9 (F) after exposure to UVB (25 and 50 mJ/cm2) in HFF1 cells (G). Representative immunoblotting image of each protein examined. The data are reported as the mean ± S.D. from two experiments performed in quadruplicates. Dashes to the right of the membrane bands show positions of prestained molecular mass markers. ** Significant vs. untreated control cells: p < 0.01; *** Significant vs. untreated control cells: p < 0.001; # Significant vs. untreated irradiated cells: p ≤ 0.05; ## Significant vs. untreated irradiated cells: p < 0.01.