Mismatched effects of receptor interacting protein kinase-3 on hepatic steatosis and inflammation in non-alcoholic fatty liver disease

Figure 3 RIP3 deletion increases hepatic fat storage. A and B: The primary hepatocytes from WT and RIP3KO mice were treated with DMSO and OA. The RIP3KO primary hepatocytes had increased Nile red staining compared to WT primary hepatocytes. RIP3 overexpression decreased Nile red staining compared to the vector group treated with OA. C and D: HepG2 cells treated with GSK'843 did not show increase Nile red staining. The expression of MTTP, PDI, and ApoB was also not decreased in GSK'843 treated HepG2 cells. E: GSK'843 treatment did not increase the expression of SREBP1c, FAS, and SCD-1 in HepG2 cells. ^aP < 0.05 by ANOVA, Duncan post hoc analysis, compared to control; ^bP < 0.05 by ANOVA, Duncan post hoc analysis. WT: Wild-type; RIP3: Receptor interacting protein kinase-3; KO: Knockout; DMSO: Dimethyl sulfoxide; OA: Oleic acid; ApoB: Apolipoprotein-B; MTTP: Microsomal triglyceride transfer protein; PDI: Protein disulfide isomerase; XBP1: X-box binding protein-1; SREBP1c: Sterol regulatory element-binding protein-1c; FAS: Fatty acid synthase; SCD-1: Stearyl-CoA desaturase-1; ANOVA, Analysis of variance.