Figure 7.

Inhibition of Giα1/3 ameliorates RGS14-deficient induced progression of NAFLD in vitro. (A) The cAMP levels in primary mouse hepatocytes transfected with indicated adenovirus with PO stimulus for 12 h (n = 3 independent experiments). (B) The protein levels of cAMP-PKA-AMPK signaling pathway in indicated groups after PO exposure, β-Actin served as an internal control (n = 3 independent experiments). (C) Representative images (n = 3 independent experiments) and quantification (n = 7 high power fields per group) of Nile Red staining of primary mouse hepatocytes transfected with indicated adenovirus under PO treatment. Scale bar, 10 um. (D) Intracellular TG content in indicated adenovirus infected primary mouse hepatocytes under the stimulation of PO (n = 3 independent experiments). (E–G) qPCR analysis of the mRNA levels of fatty acid uptake and synthesis genes (E), fatty acid oxidation genes (F) and inflammation genes (G) in infected primary mouse hepatocytes treated with PO (n = 3 independent experiments). One-way ANOVA analysis was used. ∗P < 0.05, ∗∗P < 0.01, n.s. indicates no significance between the two indicated groups. All data are shown as the mean ± s.d. Abbreviations: cAMP, cyclic adenosine monophosphate; PO, 0.5 mM Palmitic Acid and 1 mM Oleic Acid; Ad, Adenovirus; TG, Triglyceride.