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. 2020 Dec 3;10:21018. doi: 10.1038/s41598-020-78056-0

Figure 1.

Figure 1

Treatment of the FAK/PYK2 inhibitor suppresses the hepatic fibrosis in CCl4-treated mice. Four groups of mice were treated; O + Veh (n = 4), O + PF (n = 5), C + Veh (n = 9), and C + PF (n = 9). (A) The whole livers and H&E stains of liver sections (n = 4–9) from each group. Scale bar: 200 μm. Serum ALT and AST levels in each groups shown as mean ± SD (n = 4–9). (B) IHC of α-SMA (for activated HSCs; n = 4) and Sirius red (for fibrillary collagen; n = 4–9). The stained areas were shown as percentages of the total area of each liver sections (n = 4–9 in each groups). Scale bar: 200 μm in the upper row and 400 μm in the lower row. (C) qPCR of Acta2, Ctgf, Tgfb1, and Col1a1 mRNA shown as fold change compared with O + Veh control (n = in each groups). Student's t-test of C + Veh to O + Veh and C + PF to C + Veh was performed; *p < 0.05, **p < 0.01, and ***p < 0.001. O, Oil; Veh, Vehicle; C, CCl4; PF, PF-431396.