Fig. 3

Tamoxifen alleviated hepatic steatosis in MCD and CDAA-induced models. a Dosing scheme of tamoxifen on male C57BL/6 mice fed with MCD diets for 6 weeks. Dose of tamoxifen: 100 mg/kg. b Liver sections from tamoxifen group and vehicle group in mice fed with MCD diets were performed H&E, ORO, F4/80 IF, and PSR staining. H&E fat cavitation area, ORO staining area, F4/80 positive cells percentage and PSR staining area were quantitatively compared. Scale bar: 100 μm. c Dosing scheme of tamoxifen on male C57BL/6 mice fed with CDAA diets for 10 weeks. Dose of tamoxifen: 100 mg/kg. d Liver sections from tamoxifen group and vehicle group in mice fed with CDAA diets were performed H&E, ORO, F4/80 IF, and PSR staining. H&E fat cavitation area, ORO staining area, F4/80 positive cells percentage and PSR staining area were quantitatively compared. Scale bar:100 μm. e RNA was extracted from liver tissues of MCD diets-induced NASH mice administrated with tamoxifen or vehicle and expression of lipogenesis, inflammation, and fibrosis-related genes was determined by RT-qPCR with β-actin as an internal control. f RNA was extracted from liver tissues of CDAA diets-induced NASH mice administrated with tamoxifen or vehicle and expression of lipogenesis, inflammation, and fibrosis-related genes were determined by RT-qPCR with β-actin as an internal control. g Serum analysis of TC, TG, HDL and LDL in MCD diets-induced mice administrated with tamoxifen or vehicle. h Liver tissues from MCD and CDAA-induced NASH mice administrated with tamoxifen or vehicle were harvested and TG concentrations were measured using commercial kits. Hepatic TG contents were normalized by hepatic protein levels. Bars = means ± SD; n = 3–6; ns, no significance; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001