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<p>Arsenic-induced nephrotoxicity, characterized by inflammation and fibrosis, represents a critical yet inadequately addressed health concern. This study investigated the potential of ginsenoside Rg<sub>1</sub>, a bioactive component from <i>Panax ginseng</i>, to counteract arsenic-triggered renal impairment and explored the involved molecular pathways. Male C57BL/6J mice were exposed to arsenic via drinking water for 12 weeks, with a subset receiving concomitant Rg<sub>1</sub> intervention. Assessments included renal function biomarkers, histopathological evaluation of inflammation and fibrosis, and analysis of epithelial-mesenchymal transition (EMT) markers. Our findings indicated that Rg<sub>1</sub> treatment significantly ameliorated arsenic-induced renal dysfunction and pathological injury. This protection was mechanistically linked to the suppression of inflammatory responses, inhibition of fibrotic deposition and EMT process, and concomitant modulation of key pro-fibrotic signaling cascades (TGF-β1/Smad2/3, PI3K/AKT, MAPK, and AHR). In conclusion, our results demonstrated that the substantial therapeutic potential of ginsenoside Rg<sub>1</sub> against arsenic-induced kidney injury, providing a novel pharmacological perspective for intervention.</p> Graphical abstract <p></p>

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Ginsenoside Rg1 attenuates arsenic-induced nephrotoxicity in mice by suppressing inflammation, fibrosis, and EMT via multiple signalling pathways

  • 期刊论文

  • 发表日期：

    2026年6月2日

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  • Ye Li,
  • Yurong Ren,
  • Lingye Liu,
  • Xiaoming Zhang,
  • Xueyuan Zhi

摘要

Arsenic-induced nephrotoxicity, characterized by inflammation and fibrosis, represents a critical yet inadequately addressed health concern. This study investigated the potential of ginsenoside Rg1, a bioactive component from Panax ginseng, to counteract arsenic-triggered renal impairment and explored the involved molecular pathways. Male C57BL/6J mice were exposed to arsenic via drinking water for 12 weeks, with a subset receiving concomitant Rg1 intervention. Assessments included renal function biomarkers, histopathological evaluation of inflammation and fibrosis, and analysis of epithelial-mesenchymal transition (EMT) markers. Our findings indicated that Rg1 treatment significantly ameliorated arsenic-induced renal dysfunction and pathological injury. This protection was mechanistically linked to the suppression of inflammatory responses, inhibition of fibrotic deposition and EMT process, and concomitant modulation of key pro-fibrotic signaling cascades (TGF-β1/Smad2/3, PI3K/AKT, MAPK, and AHR). In conclusion, our results demonstrated that the substantial therapeutic potential of ginsenoside Rg1 against arsenic-induced kidney injury, providing a novel pharmacological perspective for intervention.

Graphical abstract