To explore the mechanism of gypenoside preventing and treating AS by affecting long non-coding RNA TUG1/miR-26a to interfere with mitochondrial apoptosis,thereby improving liver lipid deposition in ApoE^-/-AS mice.In this experiment,10 C57BL/6J mice were used as the normal control group,and 20 healthy ApoE-/-mice fed with high-fat diet for 12 weeks were randomly divided into model group and gypenoside group,given intragastrically for 4 weeks.Lipid deposition in mouse liver was observed by HE staining,blood lipid level was detected by automatic biochemical analyzer,and mRNA expression of long non-coding TUG1,miRNA-26a,Bcl2,Bax,Cytc,cleaved caspase-3,cleaved caspase-9 and cleaved PARP were detected by real-time q-PCR,and protein expression of Bcl2,Bax,Cytc,cleaved caspase-9 and cleaved PARP were detected by Wes automatic Western blotting quantitative analysis system.The results showed that the blood lipid level of ApoE-/- mice in the model group was disordered,liver cell volume increased,and fat vacuoles were obvious.The expression of Lnc-TUG1 in mouse liver was significantly increased,and miRNA-26a was significantly decreased (P<0.01);Bax,Cytc,cleaved caspase-3,cleaved PARP mRNA and protein expression significantly increased,Bcl2 mRNA and protein expression significantly decreased P<0.01 or P<0.05);cleaved caspase-9 protein expression significantly increased（P<0.05）,cleaved caspase-9 mRNA only has an upward trend.After the intervention of gypenoside,dyslipidemia was improved,the degree of liver cell steatosis was reduced,fatty vacuoles were significantly reduced.Lnc-TUG1 expression was decreased,miRNA-26a expression was increased (P<0.05),the mRNA and protein expressions of Bax,Cytc,cleaved caspase-3 and cleaved caspase-9 were significantly down-regulated,Bcl2 mRNA and protein was significantly up-regulated,the expressions of cleaved PARP protein were significantly down-regulated(P<0.01 or P<0.05),and cleaved PARP mRNA showed only a downregulation trend.The results suggested that the effect of gypenoside in preventing and treating atherosclerosis may be to interfere with mitochondrial apoptosis by affecting long non-coding RNA TUG1/miR-26a,thereby improving liver lipid deposition in ApoE^-/-AS mice.