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<p>Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder with limited treatment options. This study investigated the therapeutic potential of water extract of <i>Ajania fruticulosa</i> (WEAF) against NAFLD in cellular and animal models. WEAF significantly attenuated obesity, lipid accumulation, liver injury, and inflammation in NAFLD mice. Next, UPLC-MS/MS-based network pharmacology and molecular biology revealed that WEAF alleviated NAFLD by TLR2-mediated MYD88/NF-κB and SREBP1/PPAR-γ pathways, with 3,4-dihydroxyphenylpropionic acid, glycitein, and isorhapontigenin identified as the primary bioactive compounds. Finally, molecular docking, molecular dynamics, drug affinity responsive target stability, and cellular thermal shift assay confirmed that glycitein and isorhapontigenin directly bind to TLR2 to modulate the NF-κB/PPAR-γ signaling, and their anti-NAFLD effects were abolished by TLR2 agonist Pam3CSK4. In conclusion, WEAF and its key active compounds, glycitein and isorhapontigenin, effectively ameliorate obesity-induced NAFLD via the NF-κB/PPAR-γ signaling pathway by targeting TLR2, supporting their potential as therapeutic target and agents for NAFLD.</p>

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Computational-experimental study reveals direct target and bioactives of Ajania fruticulosa against NAFLD via TLR2/NF-κB/PPAR-γ signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月23日

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  • Chaoyue Chen,
  • Lisha Ma,
  • Awaguli Dawuti,
  • Xin Feng,
  • Shujie Chen,
  • Xueyan An,
  • Yulan Bai,
  • Tianfeng Zhang,
  • Mamatjan Aydin,
  • Kashif Kashmiri,
  • Zhancang Ma,
  • Wei Zhang,
  • Saimijiang Yaermaimaiti,
  • Abudumijiti Abulizi

摘要

Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder with limited treatment options. This study investigated the therapeutic potential of water extract of Ajania fruticulosa (WEAF) against NAFLD in cellular and animal models. WEAF significantly attenuated obesity, lipid accumulation, liver injury, and inflammation in NAFLD mice. Next, UPLC-MS/MS-based network pharmacology and molecular biology revealed that WEAF alleviated NAFLD by TLR2-mediated MYD88/NF-κB and SREBP1/PPAR-γ pathways, with 3,4-dihydroxyphenylpropionic acid, glycitein, and isorhapontigenin identified as the primary bioactive compounds. Finally, molecular docking, molecular dynamics, drug affinity responsive target stability, and cellular thermal shift assay confirmed that glycitein and isorhapontigenin directly bind to TLR2 to modulate the NF-κB/PPAR-γ signaling, and their anti-NAFLD effects were abolished by TLR2 agonist Pam3CSK4. In conclusion, WEAF and its key active compounds, glycitein and isorhapontigenin, effectively ameliorate obesity-induced NAFLD via the NF-κB/PPAR-γ signaling pathway by targeting TLR2, supporting their potential as therapeutic target and agents for NAFLD.