Mechanism and therapeutic strategy of hepatic TM6SF2-deficient non-alcoholic fatty liver diseases via in vivo and in vitro experiments

Figure 4 TM6SF2 deficiency exacerbates hepatic lipid accumulation and inflammation. A: Mice were injected with AAV-shNC and AAV-shTm6sf2 viruses via the tail vein and fed a high-fat diet or normal chow diet for 16 wk (n = 5 mice per group). The efficiency of TM6SF2 knockdown in liver were shown; B: Schematic representation of animal experiments; C: Left, representative images of hematoxylin and eosin-staining (left) and Oil Red O-staining (right) of liver sections. Right, the Nonalcoholic fatty liver disease activity score (left) and quantification of lipid (right, 8 fields of each mouse were examined) were performed; D-F: Hepatic lipid contents (triglyceride, total cholesterol and non-esterified fatty acids) (D), liver/body weight ratio (E) and body weight (F) were measured; G: Representative images of mice morphology; H: Top, representative photos of fatty livers (top) and livers subjected to magnetic resonance imaging scanning (bottom) of mice were shown. Bottom, the maximal cross-sectional area of livers is quantified by the number of pixels. ^aP < 0.05; ^bP < 0.01. NS: Not significant; H&E: Hematoxylin and eosin; NCD: Normal chow diet; HFD: High-fat diet; TG: Triglyceride; TC: Total cholesterol; NEFA: Non-esterified fatty acids.