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<p>The development of fatty liver has been associated with hepatic metabolic derangements. Genistein has been reported to be a treatment option for Non-alcoholic fatty liver disease (NAFLD). In this study, we evaluated the effect of genistein on hepatic steatosis through the silent mating type information regulation 2 homolog − 1 (SIRT1)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)/peroxisome proliferator-activated receptor α (PPARα) and Nrf2 signaling pathways in mice fed a high-fat diet (HFD). After 10 weeks of HFD feeding, the mice were randomly divided into the HFD and genistein (0.2%) groups. Genistein treatment significantly decreased liver weight and lipid accumulation in the liver of the HFD group. The mRNA level of PPARα, the acetylation of PGC-1α, mRNA, and protein levels of SIRT1 was increased in the genistein group compared with the HFD group. Genistein supplementation could enhance total antioxidant capacity, total thiol content and decrease protein carbonyl and malondialdehyde (MDA) levels in the liver of mice fed HFD. In addition, the mRNA and protein levels of Nrf2, HO-1, and SOD2 were enhanced in the liver of HFD-fed mice. These findings suggest that genistein has favorable impacts against NAFLD via activation of the SIRT1/PGC1α/PPARα and Nrf2 signaling pathways.</p>

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Genistein Has Beneficial Effects Against Non-Alcoholic Fatty Liver Disease Through Activation of the SIRT1/PPAR-α/PGC-1α and Nrf2 Signaling Pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月25日

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  • Fahimeh Zamani-Garmsiri,
  • Golnaz Goodarzi,
  • Sadra Samavarchi Tehrani,
  • ShadiSadat Seyyedebrahimi,
  • Arash Bahramzadeh,
  • Reza Meshkani

摘要

The development of fatty liver has been associated with hepatic metabolic derangements. Genistein has been reported to be a treatment option for Non-alcoholic fatty liver disease (NAFLD). In this study, we evaluated the effect of genistein on hepatic steatosis through the silent mating type information regulation 2 homolog − 1 (SIRT1)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)/peroxisome proliferator-activated receptor α (PPARα) and Nrf2 signaling pathways in mice fed a high-fat diet (HFD). After 10 weeks of HFD feeding, the mice were randomly divided into the HFD and genistein (0.2%) groups. Genistein treatment significantly decreased liver weight and lipid accumulation in the liver of the HFD group. The mRNA level of PPARα, the acetylation of PGC-1α, mRNA, and protein levels of SIRT1 was increased in the genistein group compared with the HFD group. Genistein supplementation could enhance total antioxidant capacity, total thiol content and decrease protein carbonyl and malondialdehyde (MDA) levels in the liver of mice fed HFD. In addition, the mRNA and protein levels of Nrf2, HO-1, and SOD2 were enhanced in the liver of HFD-fed mice. These findings suggest that genistein has favorable impacts against NAFLD via activation of the SIRT1/PGC1α/PPARα and Nrf2 signaling pathways.