Regulation of PPAR-γ activity in lipid-laden hepatocytes affects macrophage polarization and inflammation in nonalcoholic fatty liver disease

Figure 4 Hepatocyte-specific PPAR-γ knockout aggravates oxidative stress and NLRP3 inflammasome activation in lipid-laden hepatocytes. Primary hepatocytes were isolated from PPAR-γ^fl/fl and PPAR-γ^▲hep mice and treated with free fatty acids for 6 h for RT–PCR or 24 h for western blot, ELISA and reactive oxygen species (ROS) detection. A: mRNA expression of Ppar-γ in PPAR-γ-deficient hepatocytes; B: IL-1β production in PPAR-γ-deficient hepatocyte culture supernatant; C: ROS production in PPAR-γ deficiency hepatocytes; D: mRNA expression of NLRP3 inflammasome-related genes in PPAR-γ-deficient hepatocytes; E: Protein expression of NLRP3 inflammasome-related genes in PPAR-γ-deficient hepatocytes; F: mRNA expression of oxidative stress-related genes in PPAR-γ-deficient hepatocytes; G: Protein expression of oxidative stress-related genes in PPAR-γ-deficient hepatocytes. Values are expressed as the mean ± SE of the mean, ^aP < 0.05, ^bP < 0.01 vs ppar-γ^fl/fl or normal control-ppar-γ^fl/fl; ^cP < 0.05, ^dP < 0.01 comparison of the designated two groups, n = 3 experiments. NC: Normal control; ROS: Reactive oxygen species; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; Keap1: Kelch-like ECH-associated protein 1; Nrf2: NF-E2-related factor 2; Ho-1: Heme oxygenase-1; Nlrp3: NLR family pyrin domain-containing 3; Caspase-1: Cysteinyl aspartate-specific proteinase-1; Ppar-γ: Peroxisome proliferators-activated receptor-γ; IL: Interleukin.