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. 2020 Jul 12;11(1):100–111. doi: 10.1016/j.apsb.2020.07.004

Figure 2.

Figure 2

YD alleviated collagen accumulation and hepatic stellate cell (HSC) activation. (A) The representative photos of liver specimens with Sirius red staining and immunohistochemical staining for α-smooth muscle actin (α-SMA) and collagen type I alpha 1 (Col1a1) in oil or CCl4-induced mice with or without YD administration (n = 6/group). Liver tissues were observed by microscopy (scale bar, 50 μm). (B)–(D) Positive staining area analyses of the histological images shown in A (mean ± SD, n = 6). (E) Western blotting analyses of α-SMA and Col1a1 in mice. (F) Densitometric analyses of the blots shown in E (mean ± SD, n = 6). (G) RT-PCR analyses of genes involved in liver fibrogenesis, including α-Sma, Col1a1, Timp1, Ctgf, and Tgf-β (mean ± SD, n = 6). (H) Western blotting analyses for α-SMA and Col1a1 in LX-2 cells. (I) Densitometric analyses of the blots shown in H (mean ± SD, n = 3). ∗∗P < 0.01, ∗∗∗P < 0.001 vs. the oil or control; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. the CCl4-induced group. Area-pos, the area of positive staining; Timp1, tissue inhibitor of metalloproteinases 1; Ctgf, connective tissue growth factor; Tgf-β, transforming growth factor beta.