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<p>Calcium oxalate (CaOx), the primary constituent of most urinary calculi, triggers inflammatory responses and tissue damage upon entry into renal tubules, playing a pivotal role in nephrolithiasis pathogenesis. Salidroside (SAL), a phenolic glycoside isolated from <i>Rhodiola</i> plants, exhibits diverse pharmacological activities. This study integrated network pharmacology with experimental validation to investigate the therapeutic potential and mechanistic basis of SAL against urinary stones. In both in vitro and in vivo models of CaOx crystal-induced kidney injury, SAL treatment markedly reduced renal crystal deposition, inflammatory cascades, and associated histological impairments. Network pharmacology analysis suggested the involvement of PANoptosis, a finding subsequently confirmed through experimental assays as the central mechanism underpinning SAL-mediated protection. Molecular docking and further experimental verification indicated that SAL directly engages with core components of the PANoptosome complex. These results collectively demonstrate that SAL mitigates nephrolithiasis-related renal injury and inflammation primarily through suppression of PANoptosis.</p>

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Salidroside attenuates calcium oxalate-induced renal injury via suppression of PANoptosis

  • 期刊论文

  • 发表日期：

    2026年1月2日

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  • Guoxiang Li,
  • Zhenyu Song,
  • Junfeng Yao,
  • Yang Chen,
  • Yuexian Xu,
  • Zongyao Hao

摘要

Calcium oxalate (CaOx), the primary constituent of most urinary calculi, triggers inflammatory responses and tissue damage upon entry into renal tubules, playing a pivotal role in nephrolithiasis pathogenesis. Salidroside (SAL), a phenolic glycoside isolated from Rhodiola plants, exhibits diverse pharmacological activities. This study integrated network pharmacology with experimental validation to investigate the therapeutic potential and mechanistic basis of SAL against urinary stones. In both in vitro and in vivo models of CaOx crystal-induced kidney injury, SAL treatment markedly reduced renal crystal deposition, inflammatory cascades, and associated histological impairments. Network pharmacology analysis suggested the involvement of PANoptosis, a finding subsequently confirmed through experimental assays as the central mechanism underpinning SAL-mediated protection. Molecular docking and further experimental verification indicated that SAL directly engages with core components of the PANoptosome complex. These results collectively demonstrate that SAL mitigates nephrolithiasis-related renal injury and inflammation primarily through suppression of PANoptosis.