Western blot
1.25ug/mlPositive Control: HepG2 cell lysate
WB
(A) SIRT2 knockdown blocked PPARγ and LXRα, promoted PPARα. The GCs were transfected with SIRT2-siRNA 4 plasmids for 48 h and treated with the SIRT2 inhibitors Thiomyristoyl (2 μM) and SirReal2 (5 μM) for 24 h. Western blotting for PPARα, PPARγ, and LXRα are shown. According to the western blot results, the protein ratios were analyzed in treatment groups relative to the GAPDH protein abundance.
WB
(C) LXRα predominantly expressed in GCs, but not LXRβ. The mRNA and protein abundance of LXRα and LXRβ were respectively detected by RT-qPCR and western blot in primary GCs. The expression level of LXRβ was arbitrarily set at 1.0, and the mRNA and protein expression ratios of LXRα/ LXRβ are shown. (D) SIRT2 knockdown blocked the expression of LXRα via PPARs. The primary GCs were pretreated with SIRT2-siRNA or control siRNA for 48 h, and then treated with or without the PPARα agonist Palmitoylethanolamide (20 μM) or the PPARγ antagonist T0070907 (2 μM) for 24 h. The LXRα protein abundance was measured by western blotting. The protein ratios were analyzed in treatment groups relative to the GAPDH protein abundance.