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<p>Calcium oxalate (CaOx) stones represent the most prevalent form of urolithiasis worldwide, often leading to crystal-induced kidney injury and progressive chronic kidney disease (CKD). Hydrogen sulfide (H₂S) exhibits anti-inflammatory and antioxidant properties, but its impact on the NLRP3 inflammasome–pyroptosis axis in oxalate nephropathy remains unclear. Here, we induced oxalate nephropathy in mice using a high-oxalate, calcium-free diet and treated them with the H₂S donor sodium hydrosulfide (NaHS). NaHS administration significantly preserved renal function, reduced renal calcium crystal deposition by 78.6%, and attenuated tubular injury and fibrosis. These protective effects were accompanied by marked downregulation of NLRP3 inflammasome components, pyroptosis-related proteins, and immune cell markers CD3 and CD68 in kidney tissues. In <i>vitro</i>, NaHS suppressed oxalate-induced apoptosis and epithelial-mesenchymal transition in human proximal tubular HK-2 cells, and inhibited NLRP3 pathway activation in both HK-2 cells and macrophages. Collectively, our findings demonstrate that H₂S alleviates oxalate crystal–induced renal damage primarily by inhibiting NLRP3 inflammasome–driven inflammation and pyroptosis, highlighting its therapeutic potential in CaOx stone–related kidney injury.</p>

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Hydrogen sulfide ameliorates oxalate crystal-related renal injury via inhibiting the activation of NOD-like receptor thermal protein domain associated protein 3 inflammasome in mice

  • 期刊论文

  • 发表日期：

    2026年3月24日

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  • Yan Shi,
  • Lumiao Chen,
  • Mengqi Li,
  • Jiali Wang,
  • Peiran Yin,
  • Xun Zhou,
  • Qifei Cong,
  • Kai Song

摘要

Calcium oxalate (CaOx) stones represent the most prevalent form of urolithiasis worldwide, often leading to crystal-induced kidney injury and progressive chronic kidney disease (CKD). Hydrogen sulfide (H₂S) exhibits anti-inflammatory and antioxidant properties, but its impact on the NLRP3 inflammasome–pyroptosis axis in oxalate nephropathy remains unclear. Here, we induced oxalate nephropathy in mice using a high-oxalate, calcium-free diet and treated them with the H₂S donor sodium hydrosulfide (NaHS). NaHS administration significantly preserved renal function, reduced renal calcium crystal deposition by 78.6%, and attenuated tubular injury and fibrosis. These protective effects were accompanied by marked downregulation of NLRP3 inflammasome components, pyroptosis-related proteins, and immune cell markers CD3 and CD68 in kidney tissues. In vitro, NaHS suppressed oxalate-induced apoptosis and epithelial-mesenchymal transition in human proximal tubular HK-2 cells, and inhibited NLRP3 pathway activation in both HK-2 cells and macrophages. Collectively, our findings demonstrate that H₂S alleviates oxalate crystal–induced renal damage primarily by inhibiting NLRP3 inflammasome–driven inflammation and pyroptosis, highlighting its therapeutic potential in CaOx stone–related kidney injury.