RESUMEN
Aim To investigate whether the Adip/CaMKKp/AMPK pathway is involved in the treatment of alcoholic fatty liver in mice treated with paeonol. Methods After administration of paeonol on the basis of the mouse alcoholic fatty liver model, the inflammatory factors and TG and TC were detected by Elisa method to verify the validity of the model and drug treatment; meanwhile, the expression levels of Adip and ACC were detected by Elisa, and the nucleic acid and protein levels of Adip, CaMKK{3 and AMPKaby PCR and WB. Results Adip expression levels did not change significantly in each treatment group. Compared with control group, as for the expression of CaMKKp and AMPKa at the nucleic acid and protein-phosphorylation levels, ihe ElOH group was down-regulated to varying degrees, and the Sil and Pae groups improved the phenomenon to varying degrees. Compared with control group, as for the expression of SREBPlc at the nucleic acid and protein levels, the EtOH group was up-regulated to varying degrees, and the Sil and Pae groups improved the phenomenon to varying degrees. Conclusions The changes of theAdip/CaMKKp/AMPK signaling pathway confirm that pae-onol reduces steatosis injury of alcoholic fatty liver and inflammatory level in mice via this pathway.