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

Figure 3 Knockdown of TM6SF2 promotes intracellular lipid accumulation and lipid-overload induced cell death. A: The efficiency of TM6SF2 knockdown in two cell lines; B: Intracellular triglyceride levels (n = 3) in TM6SF2-knockdown cells were examined after palmitic acid (PA) (150 μmol/L) or bovine serum albumin (BSA) (fatty acid free) treatment for 24 h; C: Nile red staining (left, nuclei labeled with DAPI, blue) and quantification of lipid accumulation (right) of sh-Ctrl or sh-TM6SF2 L02 cells after PA or BSA treatment. Scale bars: 50 μm; D: TM6SF2-knockdown cells were incubated with PA (150 μmol/L) or BSA for 24 h. The cellular viability was examined (n = 5). ^aP < 0.05; ^bP < 0.01; ^cP < 0.001. NS: Not significant; BSA: Bovine serum albumin; PA: Palmitic acid; TG: Triglyceride; μM: μmol/L.