Effect Of MicroRNA-33on Triglyceride In HepG2Cells And The Possible Mechanisms Investigation

Objective:To investigate down-regulation and up-regulationm miRNA-33in hepG2cellsand its Effect on triglyceride and the possible mechanisms investigation.Methods:The hepG2cells were transfected with microRN-33mimics or inhibitors byLipofectamine2000. The expression of microR-33gene in the cells and transltatedcells was measured by real-time PCR. The TG content of hepG2cells was determinedafter transfected by tissue triglyceride assay kit.The relative protein expression ofAMPK was measured by Western Blot.Results:1. Compared with the control group, Transfected with microR-33a mimics groupthe content of microR-33a was increased；on the contrary， Transfected withmicroRNA-33a inhibitors group the content of microR-33a was decreased. All thechanges were statistically significant (P <0.05).2.Compared with the control group, Transfected with microR-33b mimics groupthe content of microR-33b was increased；on the contrary，Transfected withmicroR-33b inhibitors group the content of microR-33b was decreased. All thechanges were statistically significant (P <0.05).3.Compared with the control group,Respectively transfected with miR-33a/bmimics group the TG content of hepG2was increased; Conversely,Respectively transfected with miR-33a/b inhibitors group the TG content of hepG2was decreased. All the changes were statistically significant (P <0.05).4.Compared with the control group, Respectively transfected with miR-33a/b mimics group the relative protein expression of AMPK was increased andthe transfected with miR-33a/b inhibitors group was decreased. All the changes werestatistically significant (P <0.05).Conclusion:In the hepG2cells, miR-33a/b can silence the expression of AMPK bycombining AMPK to regulate triglyceride metabolism.