Abstract: To observe the effects of emodin(Emo)on acute fatty liver in mice induced by DL-ethionine(DL-Eth)or tetracyclin(Tetra)and its potential mechanism, ICR mice of acute fatty liver model induced by DL-Eth were orally administered with Emo or positive control, ursodeoxycholic acid(UDCA)for 7 days. On day 7, except that the control and Emo groups were treated with vehicle control, animals were orally administered with DL-Eth to induce acute fatty liver model. ICR mice of acute fatty liver model induced by Tetra were orally administered with Emo or positive control, Dong Bao Gan Tai (DB)or total flavonoid C-glycosides from Abrus mollis extract(AME)for 7 days. From day 4, except that the control group was treated with vehicle control, animals were injected with Tetra intraperitoneally for 4 days to induce acute fatty liver model. Liver histopathological analyses were determined by HE staining. Serum aspartate transaminase(AST), alanine transaminase(ALT), serum triglyceride(TG), hepatic TG and hepatic total cholesteol(TC)were detected. The expression of phosphorylated AMP-activated kinase(p-AMPK), phosphorylated acetyl-CoA carboxylase(p-ACC), SREBP1 and fatty acid synthase(FAS)were determined by Western blot. The expression of fatty acid translocase(CD36), peroxisome proliferator activated receptor alpha(PPARα)and microsomal triglyceride transfer protein(MTTP)in liver were determined by RT-PCR. Compared with model groups, Emo could improve hepatocyte swelling and hepatic steatosis induced by DL-Eth or Tetra. Serum AST, ALT, serum TG, hepatic TG and hepatic TC were decreased by Emo significantly. DL-Eth-induced increase of fatty acid synthetase-associated protein was down-regulated by Emo. Fatty acid uptake was down-regulated by Emo; fatty acid oxidation and secretion were increased by Emo. Emo might be effective in preventing acute fatty liver in mice induced by DL-Eth or Tetra.