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. 2014 May 6;18(6):966–974. doi: 10.1111/jcmm.12293

Figure 2.

Figure 2

Overexpression of pre-miR-483 inhibits CCl4-induced liver fibrosis in transgenic mice. (A) Haematoxylin and eosin and Masson staining of liver sections from transgenic and wild-type mice (×100/×200), immunohistochemical analysis of α-SMA and collagen1α1 (×200/×400). The results show increased collagen deposition in the transgenic mice compared to the wild-type mice, and the degree of deposition correlates with the dose of CCl4. The level of α-SMA and collagen1α1 of the WT mice are higher than in the transgenic mice. (B) The transcriptional level of α-SMA in liver. The transgenic mice presented with less α-SMA in the liver fibrosis induced by CCl4 (0.5 ml/kg). (C) The mRNA expression of collagen1α1 as determined by qRT-PCR. (D) The translationl level of α-SMA and collagen1α1 in WT and transgenic mice liver treated with low and high dose of CCl4. Overexpression of miR-483 reduced the up-regulation of α-SMA and collagen1α1 in mouse liver induced by CCl4. *P < 0.05, **P < 0.01.