IL-6上调SCD1表达对HepG2细胞脂质合成功能的影响*

doi:10.3969/j.issn.1672-5069.2019.02.005

Abstract

Abstract: Objective To investigate the upregulation of stearoyl-CoA desaturase 1（SCD1）-related lipid synthesis by IL-6 stimulus in HepG2 cells in vitro. Methods HepG2 cells were stimulated by rIL-6,and the lipid accumulation and SCD1 levels were evaluated. The SCD1 eukaryotic plasmid and small interfering RNA were conducted and transfected into HepG2 cells,respectively,and the lipid metabolism-related genes and intracellular triglyceride contents were detected. Results The intracellular triglyceride content in rIL-6-stimulated cells was significantly higher than in control group（P<0.05）;the SCD1 gene increased by 1.36 folds compared with in the control （P<0.01） and the SCD1 protein increased at the same time;the upregulation of intracellular lipid synthesis-related SREBP1c and FASN also increased by 1.35 and 1.27 folds,respectively,and the downregulation of lipid oxidation-related PPARα and ASCL3 decreased by 12.3% and 13.5%,respectively;In addition,the SCD1 transfection increased intracellular TG content in HepG2 cells（P<0.01） as compared to that in vector transfected group;conversely,after transfection with small interfering RNA and stimulation by rIL-6,the SCD1 was reduced compared with in the negative control, the intracellular TG content significantly decreased（P<0.05） and the lipid synthesis-related SREBP1c and FASN decreased by 32.3% and 51.9%, while the lipid oxidation-related PPARα also decreased by 80% （P<0.05） with the ASCL3 gene not significantly changed （P=0.832）. Conclusion rIL-6 stimulation might induce lipid synthesis and increase the triglyceride content by upregulating SCD1 expression in HepG2 cells.

Key words: HepG2 cells, Stearoyl-CoA desaturase 1, Lipid synthesis

Cao Baige, Liu Chongxiao, Chen Yuanwen, Dong Yan. Upregulation of SCD1 gene-related lipid synthesis by IL-6 stimulus in HepG2 cells in vitro[J]. JOURNAL OF PRACTICAL HEPATOLOGY, 2019, 22(2): 172-175.

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Upregulation of SCD1 gene-related lipid synthesis by IL-6 stimulus in HepG2 cells in vitro

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