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. 2022 Jan 21;177:106092. doi: 10.1016/j.phrs.2022.106092

Fig. 1.

Fig. 1

KD abolished hepatic fibro-inflammation in CCl4 mice. (A) Representative images of H&E (arrows represent inflammatory infiltrations), sirius red (arrows indicate collagenous fiber deposition), and α-SMA immunohistochmical antibody (arrows represent α-SMA expression) or Col-I immunohistochmical antibody (arrows represent Col-I expression) stained liver sections. Original magnification, 200 × ; scale bar, 100 µm. (B) Levels of ALT and AST in serum, and liver index (liver wet weight/mouse body weight×100%). (C) Serum inflammatory cytokine concentrations. (D) Transcript levels of hepatic inflammatory cytokines. (E) Content of TGF-β1, TIMP-1, TIMP-2, and MMP-13 in liver homogenate and levels of hepatic α-SMA protein. (F) Hepatic mRNA levels of α-SMA, TGF-β1, Col-I, TIMP-1, TIMP-2, and MMP-13. Data expressed as mean ± SD (n = 6). *P < 0.05, **P < 0.01 relative to controls; #P < 0.05, ##P < 0.01 relative to CCl4-induced LF mice.