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<p>Peritoneal fibrosis (PF) is a major complication of long-term peritoneal dialysis (PD). This study investigated the protective effects and mechanisms of asiaticoside (AC) against PF. In vitro, HMrSV5 cells were exposed to peritoneal dialysis fluid (PDF) with or without AC, and assessed for viability, migration, fibrosis/mesothelial-to-mesenchymal transition (MMT) markers (α-smooth muscle actin (α-SMA), Collagen I, E-cadherin, Vimentin), reactive oxygen species (ROS), mitochondrial membrane potential, and aryl hydrocarbon receptor (AhR) transcriptional activity using a dual-luciferase reporter assay. Subcellular localization of AhR was evaluated to examine nuclear translocation, and AhR overexpression was employed to confirm pathway dependence and its interaction with nuclear factor erythroid 2 related factor 2 (Nrf2). In vivo, mice received daily intraperitoneal 4.25% PDF with or without oral AC (50 or 100&#xa0;mg/kg), and peritoneal function, histology, and α-SMA/Collagen I expression were quantified. AC co-treatment significantly inhibited PDF-induced MMT, oxidative stress, mitochondrial dysfunction, and AhR nuclear translocation, while enhancing Nrf2 nuclear accumulation; AhR overexpression partially reversed these effects. In mice, AC preserved peritoneal function, reduced fibrosis, and modulated AhR–Nrf2 signaling. These results demonstrate that AC protects against PDF-induced PF by suppressing AhR activation and promoting Nrf2 nuclear translocation, indicating its protective effects in preclinical models of PD-associated PF.</p>

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Asiaticoside protects against PDF-induced peritoneal fibrosis via suppression of AhR/Nrf2-mediated MMT and oxidative stress

  • 期刊论文

  • 发表日期：

    2025年12月26日

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  • Junyi Zhao,
  • Wen Zhou,
  • Wenxuan Xue,
  • Mengyun Yuan,
  • Mengya Wang,
  • Zhichen Cai,
  • Ning Ding

摘要

Peritoneal fibrosis (PF) is a major complication of long-term peritoneal dialysis (PD). This study investigated the protective effects and mechanisms of asiaticoside (AC) against PF. In vitro, HMrSV5 cells were exposed to peritoneal dialysis fluid (PDF) with or without AC, and assessed for viability, migration, fibrosis/mesothelial-to-mesenchymal transition (MMT) markers (α-smooth muscle actin (α-SMA), Collagen I, E-cadherin, Vimentin), reactive oxygen species (ROS), mitochondrial membrane potential, and aryl hydrocarbon receptor (AhR) transcriptional activity using a dual-luciferase reporter assay. Subcellular localization of AhR was evaluated to examine nuclear translocation, and AhR overexpression was employed to confirm pathway dependence and its interaction with nuclear factor erythroid 2 related factor 2 (Nrf2). In vivo, mice received daily intraperitoneal 4.25% PDF with or without oral AC (50 or 100 mg/kg), and peritoneal function, histology, and α-SMA/Collagen I expression were quantified. AC co-treatment significantly inhibited PDF-induced MMT, oxidative stress, mitochondrial dysfunction, and AhR nuclear translocation, while enhancing Nrf2 nuclear accumulation; AhR overexpression partially reversed these effects. In mice, AC preserved peritoneal function, reduced fibrosis, and modulated AhR–Nrf2 signaling. These results demonstrate that AC protects against PDF-induced PF by suppressing AhR activation and promoting Nrf2 nuclear translocation, indicating its protective effects in preclinical models of PD-associated PF.