Study On The Mechanism Of C1q/Tumor Necrosis Factor-related Protein-3 Regulating LDLR Expression Through AKT Signaling Pathway In HepG2 Cells

Objective:1.Effects of C1q/TNF-related proteins-3 on Low density lipoprotein receptor expression of HepG2 cells.2.The specific mechanism of C1q/TNF-related proteins-3 affects Low density lipoprotein receptor expression.3.Whether C1q/TNF-related proteins-3 regulates Low density lipoprotein receptor expression through the AKT signaling pathway.Method:1.Grouping:(1)the control group(2)Different concentrations of CTRP3(0?1?3?10mg/L)intervention group(intervention 36 hours)(3)At different times(12?24?36h),CTRP3 intervention group(intervention concentration 3mg/L)(4)LY294002(10umol)intervention group(5)LY294002(10umol)+ CTRP3(3mg/L)intervention group2.The expression of LDLR,SREBP1 and PCSK9 in HepG2 cells was detected by Western Blotting and RT-PCR.Results:1.CTRP3 could promote the expression of LDLR on HepG2 cells.RT-PCR andWestern blot showed that the mRNA and protein expressions of LDLR,SREBP1 and PCSK9 in CTRP3 group were significantly higher than those in control group(P<0.05).With the increase of CTRP3 concentrations(0,1,3,10 mg / L),the expression of LDLR,SREBP1 and PCSK9 has increased.2.CTRP3 promotes LDLR expression via the AKT signaling pathway: CTRP3 increases AKT activation and LDLR expression in cultured HepG2 cells,and appears to be time and dose-dependent.In addition,CTRP3 failed to increase LDLR expression in HepG2 cells when we blocked AKT signaling with AKT inhibitors Conclusion:1.CTRP3 could promote the expression of LDLR on HepG2 cells.2.CTRP3 promotes LDLR synthesis to increase its expression level.3.CTRP3 promotes LDLR expression via the AKT signaling pathway.