Synergistic effect on nonalcoholic fatty liver disease by aptamer functionalized liposome loading allicin

• Allicin prevents and reverses NAFLD and obesity. • LAA is more effective in reversing NAFLD compared with free allicin. • The findings suggest that LAA intervention ameliorate hepatic lipid metabolism disorders and alleviate NAFLD by inhibiting the expression of key genes for lipid synthesis. Nonalcoholic fatty liver disease (NAFLD) is a global public health problem with no clinically specific drug. Therefore, it is critical to develop safe and effective drugs with minimal side effects for the treatment of NAFLD. In this study, we constructed aptamer-functionalized liposome, namely LAA (liposome-allicin-aptamer), targeted to NAFLD cell to effectively deliver allicin to improve NAFLD. Our in vitro results showed that allicin loaded in liposome reduced oleic acid-induced intracellular lipid droplet accumulation and triglyceride synthesis in HepG2 cells. In vivo , it also significantly reduced lipid accumulation and improved liver injury in high fat diet induced obesity (DIO) mice. In addition, allicin was found to reduce the expression of genes involved in lipid synthesis, include acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD-1), sterol regulatory element binding protein 1-C (SREBP1-C), and peroxisome proliferator-activated receptor-γ (PPARγ) in vitro and in vivo . Markedly, the LAA showed superior performance in improving NAFLD compared with free allicin, that provide a new strategy for the delivery of allicin.