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作 者:HUANG Xiao‑xia ZHENG Zhi‑min PANG Bi‑ying HUANG Na‑na LI Xin XIONG Wen‑ting KONG Bo LIU Ji‑sheng
机构地区:[1]School of Life Sciences,Guangzhou University,Guangzhou 510006,China
出 处:《Journal of Hainan Medical University》2023年第12期10-17,共8页海南医学院学报(英文版)
基 金:National Natural Science Foundation of China(81973376)。
摘 要:Objective:To investigate the regulatory mechanism in liver fibrosis progression by nuclear receptor of farnesoid X receptor(FXR)and the lipid droplet-associated protein of perilipin 5(PLIN5).Methods:FXR response element(FXRE)upstream of PLIN5 gene was found by bioinformatics,and confirmed by a dual luciferase reporter gene system;a hepatic fibrosis model based on human hepatic stellate cell LX-2 was established by induction of transforming growth factor-β1(TGF-β1);mRNA and protein levels ofα-smooth muscle actin(α-SMA)and collagen栺were measured by qPCR and Western blot after transient overexpression of FXR or PLIN5;Oil red O staining was used to study the formation of lipid droplets.Results:The promoter region of the PLIN5 gene contained a known reverse repeats-1(IR-1);the gene expression of PLIN5 in LX-2 cells was up-regulated after FXR activation(P<0.01);overexpression of PLIN5 promoted the formation of lipid droplets and significantly reduced the TGF-β1 induced fibrosis gene expression(P<0.05);FXR activation showed no effects on the inhibition of LX-2 cells activation.Conclusion:Overexpression of PLIN5 promotes the formation of lipid droplets and inhibits activation of LX-2 cells.FXR might bind to the FXRE site upstream of PLIN5 gene and regulate its gene expression.In summary,FXR may prevent liver fibrosis progression partially by regulating lipid droplet-associated protein of PLIN5.
关 键 词:Farnesoid x receptor PLIN5 Lipid droplet Hepatic stellate cell Liver fibrosis
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