To explore the molecular mechanism of the regulation of PPARα level and lipidlowering in Tibetan tea aqueous extract, the prokaryotic recombinant vector pET32a-PTD-PPAR was constructed to express PTD-PPARα fusion protein with cellentering ability, and constructed of a highlipid cell model using hepatocyte Lo2 cell line. SDS-PAGE and Western blotting results indicated that PTD-PPARα fusion protein had a high purity and specificity, and it could enter L02 cells and reduce lipid deposition in L02 highfat cells. The L02 highfat cell model was treated with Tibetan tea aqueous extract for 24 h, lipid deposition analyzed by Oil red O staining showed that cell lipid deposition was significantly decreased; western blotting also showed PPARα protein levels increased significantly with a concentrationdependent manner. In conclusion, the results showed that the aqueous extract of Tibetan tea may inhibit the deposition of lipids in cells by regulating the level of PPARα protein and regulate lipid metabolism.