Fig. 3
AMPK inhibition hampered the protective effect of AAV2/8 CAV1 treatment on LD-induced hepatic lipid accumulation
Mice were injected (either via the i.v. or i.p. route) with or without AAV2/8CAV1 at 1 × 1011 vg/animal and then fed LD. n = 13 for each group, LD-fed mice with either i.v. or i.p. administration of AAV2/8CAV1 with or without compound c treatment (10 mg/kg, i.p. injection once a day); n = 9 for LD-fed mice (control) with neither AAV2/8CAV1 administration nor compound c treatment
The letters on each bar are provided for statistical purposes, and different letters indicate significance (P < 0.05). If there are no significant differences between two bars, they have the same letter. The individual P values are described in Supplementary Table 3.
A. Quantitation of free fatty acids, triacylglycerol, and cholesterol in the liver of each group of mice.
B. Proportion of each liver free fatty acid profile (palmitic acid, stearic acid, oleic acid, linoleic acid, and arachidonic acid) in each group of mice.
C. Western blotting analysis of AMPK (and its phosphorylation), CAV1, and SREBP1c protein expression in the liver and gallbladder of each group of mice. β-actin was used as a loading control. Data are representative of three samples for each protein. T172, the activation marker of AMPK phosphorylation at threonine 172; i.v., AAV2/8CAV1 injection (1 × 1011 vg/mice) via the i.v. route; i.p., AAV2/8CAV1 injection (1 × 1011 vg/mice) via the i.p. route; CC, compound C injection (10 mg/kg/day) via the i.p. route.