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Updated: Jan 22, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

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Celastrol attenuates ox-LDL-induced mesangial cell proliferation via suppressing NLRP3 inflammasome activation

Zhenzhen Sun1,2,3, Yuanyuan Li1,2,3, Yun Qian1,2,3

  • 11Department of Nephrology, Children's Hospital of Nanjing Medical University, Guangzhou Road #72, 210008 Nanjing, China.

Cell Death Discovery
|July 10, 2019
PubMed

Insights

Celastrol inhibits mesangial cell proliferation and NLRP3 inflammasome activation induced by oxidized LDL. This suggests celastrol may treat obesity-related kidney disease and proliferative glomerular disorders.

Area of Science:

  • Nephrology
  • Immunology
  • Pharmacology

Background:

  • Mesangial cell (MC) proliferation is a key feature of obesity-associated nephropathy, potentially leading to glomerulosclerosis and kidney dysfunction.
  • Targeting MC proliferation offers a therapeutic strategy for obesity-related kidney disease.

Purpose of the Study:

  • To investigate celastrol's role in inhibiting oxidized low-density lipoprotein (ox-LDL)-induced MC proliferation.
  • To elucidate the underlying mechanisms involving the NLRP3 inflammasome.

Main Methods:

  • MCs were treated with ox-LDL, with or without celastrol pretreatment.
  • NLRP3 inflammasome activation was assessed by measuring NLRP3 levels, caspase 1 activity, and IL-1β/IL-18 release.
  • MC proliferation and cell cycle progression were evaluated using cell cycle assays and cyclin A2/D1 expression analysis.
  • NLRP3 inflammasome was inhibited using NLRP3 siRNAs.

Main Results:

  • Ox-LDL treatment induced MC proliferation and activated the NLRP3 inflammasome.
  • NLRP3 siRNA significantly inhibited MC proliferation and delayed cell cycle progression.
  • Celastrol pretreatment markedly suppressed ox-LDL-induced NLRP3 inflammasome activation and MC proliferation.

Conclusions:

  • Celastrol effectively inhibits ox-LDL-induced mesangial cell proliferation, likely by suppressing NLRP3 inflammasome activation.
  • Celastrol shows potential as a therapeutic agent for obesity-related proliferative glomerular diseases and lipid disorders.
Keywords:
Cell biologyKidney diseases

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