Figure 8. MiR-378a-3p promotes inactivation of HSC in CCl₄-treated mice.

(a) qRT–PCR analysis for α-sma, vimentin, col1α1 and timp1 in NP/NC, CCl₄, CCl₄+NPs/NC and CCl₄+NPs/M group (n=4 per group). All results of relative expression values are shown as mean±s.e.m. (Kruskal–Wallis test and unpaired two-sample Student's t-test, *P<0.05 and **P<0.005 versus NP/NC). (b) Western blot analysis for α-SMA (42 kDa), GFAP (50 kDa) and GAPDH (36 kDa) in livers of representative mice from each group. Data shown represent one of three experiments with similar results. (c) Cumulative densitometric analyses of α-SMA and GFAP western blotting results are displayed as the mean±s.e.m. (Kruskal–Wallis test and unpaired two-sample Student's t-test, *P<0.05 and **P<0.005). (d) Immunohistochemistry for α-SMA in liver sections from representative NP/NC, CCl₄, CCl₄+NPs/NC and CCl₄+NPs/M group (scale bar, 100 μm).