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Background <p>Amygdalin (Amy) exhibits multiple pharmacological properties, including anti-fibrotic and anti-inflammatory effects, but its protective role against Hyperuricemia (HUA)-related kidney injury remains unclear.</p> Objectives <p>To investigate whether Amy improves HUA by regulating the reactive oxygen species (ROS)/NLRP3 axis.</p> Results <p>Amy lowered serum LDH levels in HUA mice, improved renal function indicators, and alleviated renal tissue pathological damage and fibrosis. Amy effectively reduced ROS and inflammatory factor levels in the kidney tissue of HUA mice, alleviating macrophage infiltration and oxidative stress. Concurrently, Amy enhanced the viability of NRK-52E cells after UA induction while reducing LDH activity and cell death rates, thereby alleviating inflammatory and oxidative stress. Mechanistically, Amy hindered NLRP3 inflammasome activation and down-regulated pyroptosis-associated proteins. The ROS-inducing activator 3-NPA/rotenone reversed the aforementioned protective effect, elevating ROS levels and pyroptosis-related protein expression.</p> Conclusions <p>Amy mitigates UA-induced damage to NRK-52E cells and renal injury in mice by hindering ROS production and blocking NLRP3 inflammasome-mediated pyroptosis.</p>

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Amygdalin mitigates renal injury in hyperuricemic mice by modulating ROS/NLRP3-induced pyroptosis

  • 期刊论文

  • 发表日期：

    2026年6月22日

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  • Xiaoliang Wang,
  • Siyi Chen,
  • Xiaoyi Sun,
  • Qianpan Liu,
  • Yue Wang,
  • Xiang Li,
  • Weixin Kong,
  • Chunbo Zou

摘要

Background

Amygdalin (Amy) exhibits multiple pharmacological properties, including anti-fibrotic and anti-inflammatory effects, but its protective role against Hyperuricemia (HUA)-related kidney injury remains unclear.

Objectives

To investigate whether Amy improves HUA by regulating the reactive oxygen species (ROS)/NLRP3 axis.

Results

Amy lowered serum LDH levels in HUA mice, improved renal function indicators, and alleviated renal tissue pathological damage and fibrosis. Amy effectively reduced ROS and inflammatory factor levels in the kidney tissue of HUA mice, alleviating macrophage infiltration and oxidative stress. Concurrently, Amy enhanced the viability of NRK-52E cells after UA induction while reducing LDH activity and cell death rates, thereby alleviating inflammatory and oxidative stress. Mechanistically, Amy hindered NLRP3 inflammasome activation and down-regulated pyroptosis-associated proteins. The ROS-inducing activator 3-NPA/rotenone reversed the aforementioned protective effect, elevating ROS levels and pyroptosis-related protein expression.

Conclusions

Amy mitigates UA-induced damage to NRK-52E cells and renal injury in mice by hindering ROS production and blocking NLRP3 inflammasome-mediated pyroptosis.