Fig. 12. WA treatment improved serum and liver biochemical parameters and reduced HFD-induced hepatic fibrosis and mRNAs associated with ER stress and ceramide biosynthesis and catabolism in WA-treated HFD-fed ob/ob mice. (A–F) Analysis of liver TG levels (A), TC levels (B), NEFA levels (C), serum TG (D), serum TC (E), and serum NEFA levels (F). (G) Hepatic fibrosis marker analysis of Timp2, Col1a1, Mmp2, and Acta2 mRNA levels. (H) Representative hepatic picrosirius red staining for HFD and WA-treated HFD livers. Scale bar, 100 μm. (I) Hepatic endoplasmic reticulum stress signaling marker analysis of Hspa5 and Didt3 mRNA levels. (J) Sptlc1, Sptlc2, Smpd2, Smpd3, Acer1, Acer2, Sgms1, Sgms2, Cers2, Cers4, and Cers6 mRNA levels. Data were presented as means ± S.D. NV, mice fed the HFD-induced NASH diet (N) and treated with vehicle (V) for 12 weeks. N+WA5, mice fed the HFD-induced NASH diet and treated with 5 mg/kg WA for the last 4 weeks n = 5 mice for the HFD-fed vehicle groups and n = 8 for WA treated HFD-fed ob/ob mice. *P < 0.05; **P < 0.01; ***P < 0.005 compared with HFD group. Statistical differences were determined by the two-tailed t test.