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<p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is considered an important independent risk factor for hepatocellular carcinoma. This study aims to investigate the anti-lipogenic effects and mechanisms of Malvidin-3,5-<i>O</i>-diglucoside (M35G) derived from <i>Vitis davidii</i> on a high-fructose-induced MASLD cell model in HepG2 cells. Through the detection of various physicochemical indicators, histology, free fatty acids and their metabolites, transcription factors, and enzyme expression, it was demonstrated that 10 mM fructose treatment for 72 h significantly increased lipid accumulation in HepG2 cells. M35G reduced hepatic lipid accumulation and improves free fatty acids metabolism by inhibiting the expression of transcription factors and enzymes involved in de novo lipogenesis and promoting the β-oxidation of fatty acids. M35G also ameliorated fructose-induced glucose metabolism disorder by suppressing ketohexokinase-c and phosphoenolpyruvate carboxykinase expression while upregulating adenosine 5’-monophosphate-activated protein kinase and pyruvate kinase M2 isoform expression. This validated the inhibitory role of M35G in mediating the development of fatty liver disease, which may aid in the prevention and treatment of MASLD.</p>

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Malvidin-3,5-O-diglucoside derived from spine grape (Vitis davidii) inhibits fructose-induced lipid accumulation in HepG2 cells: beneficial effects on MASLD treatment

  • 期刊论文

  • 发表日期：

    2025年10月29日

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  • Tiantian Cheng,
  • Yang Liu,
  • Yifan Wang,
  • Pei Zhao,
  • Xinyuan Ma,
  • Fuliang Han

摘要

Metabolic dysfunction-associated steatotic liver disease (MASLD) is considered an important independent risk factor for hepatocellular carcinoma. This study aims to investigate the anti-lipogenic effects and mechanisms of Malvidin-3,5-O-diglucoside (M35G) derived from Vitis davidii on a high-fructose-induced MASLD cell model in HepG2 cells. Through the detection of various physicochemical indicators, histology, free fatty acids and their metabolites, transcription factors, and enzyme expression, it was demonstrated that 10 mM fructose treatment for 72 h significantly increased lipid accumulation in HepG2 cells. M35G reduced hepatic lipid accumulation and improves free fatty acids metabolism by inhibiting the expression of transcription factors and enzymes involved in de novo lipogenesis and promoting the β-oxidation of fatty acids. M35G also ameliorated fructose-induced glucose metabolism disorder by suppressing ketohexokinase-c and phosphoenolpyruvate carboxykinase expression while upregulating adenosine 5’-monophosphate-activated protein kinase and pyruvate kinase M2 isoform expression. This validated the inhibitory role of M35G in mediating the development of fatty liver disease, which may aid in the prevention and treatment of MASLD.