陆军军医大学学报 (Feb 2023)

Equol intervention ameliorates steatosis in HepG2 cells induced by sodium oleate

  • ZHANG Guiming,
  • NI Xiangmin,
  • CUI Hanqiang,
  • XU Zhe,
  • LI Shuo

DOI
https://doi.org/10.16016/j.2097-0927.202207014
Journal volume & issue
Vol. 45, no. 3
pp. 202 – 208

Abstract

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Objective To observe the effect of equol (Eq) intervention on sodium oleate (NaOL)-induced steatosis in HepG2 cells and study its mechanism of action. Methods HepG2 cells were treated with different concentrations of NaOL (0, 0.12, 0.24, 0.36, 0.48, 0.60 and 0.72 mmol/L) for 48 h to induce cell steatosis. Oil red O staining was used to observe the accumulation of intracellular lipid droplets, and triglyceride (TG) content was measured. CCK-8 assay was employed to determine the optimal concentration of NaOL in the inducement of hepatic steatosis and the concentration range for Eq intervention. Then HepG2 cells were randomly divided into 6 groups: control group, NaOL group, NaOL+low-, medium- and high-dose Eq groups (10-7, 10-6, and 10-5 mol/L), NaOL+estradiol intervention group (E2, 10-7 mol/L). After Eq intervention for 48 h, cellular TG content was detected, and Oil red O staining was adopted to observe the accumulation of intracellular lipid droplets, and the expression of SREBP-1c, FAS, PPARα and CPT-1A at mRNA and protein levels was detected by qRT-PCR and Western blotting, respectively. Results NaOL of 0.24 mmol/L showed no significant effect on the viability of HepG2 cells, but significantly increased intracellular TG content and accumulated a large number of lipid droplets. Compared with the NaOL group, Eq or E2 intervention reduced the intracellular lipid droplet accumulation in HepG2 cells induced by NaOL, significantly decreased the intracellular TG content (P<0.05), down-regulated the mRNA and protein expression levels of SREBP-1c and FAS (P<0.05), and up-regulated those of PPARα and CPT-1A (P<0.05). Conclusion Eq could effectively improve NaOL-induced steatosis in HepG2 cells, and it may be related to its inhibiting SREBP-1c and FAS expression, while enhancing PPARα and CPT-1A expression.

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