FAT/CD36受体识别转运LCFA和oxLDL、SREBPs上调TG和TC合成途径，是NAFLD脂质代谢异常发生的关键病理环节。寻求靶向竞争结合FA/CD36，调控SREBP-1c 和SREBP-2脂质合成，实施NAFLD早期干预保护至关重要。前期研究发现并报道小分子先导化合物（OXL01）以ω-COOH基团为活性中心与FAT/CD36形成分子稳定最低能量结合；下调SREBP-1c 和SREBP-2及其下游靶基因表达；显著降低C57BL/6小鼠肝脏TG和TC异位沉积。提示OXL01可能以亲和配体形式作用于FAT/CD36及其下游途径，特异性调控脂质合成途径达到降脂作用的重要意义。本课题拟运用FAT/CD36及其下游基因过表达、siRNA和慢病毒注射，研究OXL01与FAT/CD36的结合关系以及调控SREBPs及其下游靶基因失稳态分子机理，探讨OXL01的NAFLD生物学保护作用。

FAT / CD36 receptor recognition and transport for LCFA and oxLDL, and sterol regulatory element binding proteins（SREBPs）increase TG and TC synthetic are important pathological events of NAFLD. It seems is essential for targeted competition binding FAT / CD36 and.regulation SREBP-1c and SREBP-2 lipid synthesis in early protection of NAFLD. Our latest research reported a small molecule Lead compounds-OXL01 in ω-COOH group active center which could specifically bind FAT / CD36 to forming a stable lowest energy combination . It can inhibited the gene and protein expression of SREBP-1c and SREBP-2 and its downstream target genes in vitro. It can also significantly reduced triglyceride and cholesterol in HepG2 cell and C57BL/6 mice when treated with OXL01 chronically. It is very important that all of them imply OXL01 may is an affinity ligand of FAT / CD36, and OXL01 reduced triglyceride and cholesterol by suppressing pathway of FAT / CD36 and its downstream gene. This paper intends to research the binding relationship the OXL01 and FAT / CD36, and the OXL01 regulating molecular mechanism of lipid disorder by pathway of SREBPs and downstream target genes. Explore the biological protective effects of OXL01 in NAFLD.