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. Author manuscript; available in PMC: 2018 Jan 1.
Published in final edited form as: Gastroenterology. 2017 Oct 4;154(1):238–252.e7. doi: 10.1053/j.gastro.2017.09.022

Fig. 1. Treatment with rAAV8-MIR122-OX protects from ALD by restoring the alcohol-induced reduction of MIR122 expression.

Fig. 1

Expression of MIR122 in (A)human livers (n=9–12/group), (B)murine livers (n=8–14/group), murine hepatocytes and liver mononuclear cells (LMNCs) of pair-fed and alcohol-fed mice (n=5/group). Hepatic (C)MIR122 expression, from livers of either Et-fed WT mice treated with rAAV8-Scr or rAAV8-MIR122-OX vectors (n=8–12/group). Liver injury, inflammation, and steatosis was assessed by (D) serum ALT, liver MCP-1 and IL-1β protein levels, and (E) H&E, ORO staining, hepatic triglycerides concentrations, respectively. (F)ALT at 0-, 24-, and 48-hours following final dose of CCl4(n=6–10). Hepatic fibrosis was evaluated by measuring (G)Sirius-red staining and the percent-positive area stained was quantified using ImageJ and (H)Col1a1 and Acta2 expression from total liver RNA (n=6–10). Scale bars; 100 μm. Student’s t-test or two-way ANOVA.