Morroniside Delays NAFLD Progression in Fructose-Fed Mice by Normalizing Lipid Metabolism and Inhibiting the Inflammatory Response

Figure 5

Morroniside normalizes lipid metabolic disorder in vitro. (a) Morroniside attenuated fructose-induced lipid accumulation in HepG2 cells by Nile red staining. (b) Morroniside reduced triglyceride (TG) content in fructose-induced HepG2 cells. (c, d) Representative immunoblots and quantification of key proteins in lipogenesis (PGC1β, p-SREBP-1 (precursor), n-SREBP-1 (nuclear), FASN, and ACC) and fatty acid oxidation (PPARα and CPT1α) in the fructose-induced HepG2 cells. (e, f) Representative immunoblots and quantification of key proteins in lipogenesis (PGC1β, p-SREBP-1 (precursor), n-SREBP-1 (nuclear), FASN, and ACC) and fatty acid oxidation (PPARα and CPT1α) in the fructose-induced AML-12 cells. (g, h) Representative immunoblots and quantification of p-SREBP-1 (precursor), n-SREBP-1 (nuclear), FASN, PPARα, and CPT1α in fructose-treated HepG2 cells by morroniside under PGC1β overexpression. Mean ± S.D., n = 3, ^##, ^### vs. the con group; , , vs. the fructose-treated group; ^⧫, ^⧫⧫, ^⧫⧫⧫ vs. the fructose and morroniside coprocessing group. Con: control.

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)