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Abstract <p><b>Objective:</b> The natural anthraquinone emodin exhibits multiple pharmacological effects, including anti-inflammatory and anti-fibrotic properties. However, its therapeutic potential and mechanism of action in alcoholic liver fibrosis (ALF) remain insufficiently explored. <b>Methods:</b> The therapeutic effect of emodin was evaluated in a mouse model of ALF induced by chronic ethanol feeding and in ethanol-exposed hepatic stellate cells (HSC-T6) <i>in vitro</i>. Serum biochemistry, liver histopathology, and the expression of fibrosis-related markers were assessed. <b>Results and Discussion:</b> <i>In vitro</i>, emodin dose-dependently inhibited the proliferation and promoted the apoptosis of ethanol-exposed HSC-T6 cells. <i>In vivo</i>, emodin treatment significantly reduced serum ALT and AST levels, attenuated histopathological damage, and decreased collagen deposition in ALF mice. Molecular analyses revealed that emodin downregulated miR-21 expression and upregulated the expression of its target, ADAMTS-1. Emodin treatment also inhibited the TGF-β1/Smad3 signaling pathway and shifted the balance of extracellular matrix regulators by decreasing TIMP-1 and increasing MMP-2 expression in both models. <b>Conclusions:</b> Emodin demonstrates potent anti-fibrotic effects in experimental ALF. Its mechanism is associated with the inhibition of the TGF-β1/Smad3 pathway, modulation of the miR-21/ADAMTS-1 axis, and restoration of the MMP-2/TIMP-1 balance, leading to enhanced matrix degradation. These findings highlight emodin as a promising candidate for further investigation in the treatment of alcoholic liver fibrosis.</p>

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Emodin Alleviates Alcohol-Induced Liver Fibrosis by Modulating Extracellular Matrix and Inhibiting the TGF-β1/Smad3 Signaling Pathway

  • 期刊论文

  • 发表日期：

    2026年2月12日

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  • Bingbing Zhang,
  • Mengli Yang,
  • Sanqiang Li,
  • Longfei Mao,
  • Xiaomin Hong,
  • Renli Luo,
  • Ruifang Li,
  • Qinyi Cui

摘要

Abstract

Objective: The natural anthraquinone emodin exhibits multiple pharmacological effects, including anti-inflammatory and anti-fibrotic properties. However, its therapeutic potential and mechanism of action in alcoholic liver fibrosis (ALF) remain insufficiently explored. Methods: The therapeutic effect of emodin was evaluated in a mouse model of ALF induced by chronic ethanol feeding and in ethanol-exposed hepatic stellate cells (HSC-T6) in vitro. Serum biochemistry, liver histopathology, and the expression of fibrosis-related markers were assessed. Results and Discussion: In vitro, emodin dose-dependently inhibited the proliferation and promoted the apoptosis of ethanol-exposed HSC-T6 cells. In vivo, emodin treatment significantly reduced serum ALT and AST levels, attenuated histopathological damage, and decreased collagen deposition in ALF mice. Molecular analyses revealed that emodin downregulated miR-21 expression and upregulated the expression of its target, ADAMTS-1. Emodin treatment also inhibited the TGF-β1/Smad3 signaling pathway and shifted the balance of extracellular matrix regulators by decreasing TIMP-1 and increasing MMP-2 expression in both models. Conclusions: Emodin demonstrates potent anti-fibrotic effects in experimental ALF. Its mechanism is associated with the inhibition of the TGF-β1/Smad3 pathway, modulation of the miR-21/ADAMTS-1 axis, and restoration of the MMP-2/TIMP-1 balance, leading to enhanced matrix degradation. These findings highlight emodin as a promising candidate for further investigation in the treatment of alcoholic liver fibrosis.