| Objective Clarify the inhibitory effect of salvianolic acid A on the accumulation of lipid in liver cells,and elucidate the mechanism of its inhibition of lipid accumulation.Providing a new theoretical basis for the clinical treatment of ALD.It provides new ideas for the development of new drugs based on SAA for the treatment of ALD.Methods Twenty-four C57BL/6 mice were randomized into 3 equal groups;Control group,ALD group,SAA injection group.Mice were fed Lieber-DeCarli diet-The level of ALT and TG were measured by relative kits.The level of PPARa were measured by Western blot.HepG2 were randomized into 4 equal groups,UT group,SAA group,OA group,OA+SAA group.The level of lipid in HepG2 were measured by Oil Red stain and the level of TG were measured by relative kits.The level of PPARa were measured by Western blot and the gene of PPARα,FALDH,DGAT,CPT1 were measured by Realtime PCR.Results ①ALD mouse model were built successfully.②SAA significantly decreased the level of TG and lipid in mouse liver and HepG2.③SAA significantly decreased the level of TG and ALT in serum of mouse.④SAA significantly increased the level of PPARa in mouse liver and HepG2.⑤SAA significantly increased the level of target gene of PPARα,FALDH.Conclusion Supplementation of SAA,confered a protective effect on alcoholic-induced liver injury in mice,and inhibited the accumulation of lipid in HepG2.The protective effect of SAA was associated with actived hepatic PPARα,FALDH,and dcreased hepatic lipid accumulation. |