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Updated: Feb 3, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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[Soluble Uric Acid Activates NLRP3 Inflammasome in Myocardial Cells Through Down-regulating UCP2]

Guan-Li Wang1, Hong-Min Yuan2, Zhen-Feng Wang1

  • 1Henan Key Laboratory of Cellular and Molecular Immunology, Joint National Laboratory for Antibody Drug Engineering, Henan University, Kaifeng 475004, China.

Sichuan Da Xue Xue Bao. Yi Xue Ban = Journal of Sichuan University. Medical Science Edition
|November 1, 2018
PubMed
Abstract

Insights

Soluble uric acid (UA) causes H9C2 cell damage by down-regulating UCP2, damaging mitochondria, and activating the NLRP3 inflammasome. NAC treatment mitigated these effects, improving cell viability.

Area of Science:

  • Cardiovascular Research
  • Cellular Biology
  • Biochemistry

Background:

  • Soluble uric acid (UA) is implicated in cardiovascular disease.
  • The role of UA in H9C2 cell damage and NLRP3 inflammasome activation requires further elucidation.

Purpose of the Study:

  • To investigate the effects of soluble uric acid (UA) on H9C2 cell damage.
  • To determine the impact of UA on NLRP3 inflammasome activation and mitochondrial function.

Main Methods:

  • H9C2 cells were treated with UA, and cellular damage was assessed via MTS and LDH assays.
  • Apoptosis, NLRP3 inflammasome components (NLRP3, ASC, Caspase-1), mitochondrial damage (cytochrome C release), and UCP2 expression were analyzed.
  • The effects of N-acetylcysteine (NAC), a reactive oxygen species (ROS) inhibitor, were evaluated.

Main Results:

  • UA induced dose- and time-dependent H9C2 cell damage and apoptosis.
  • UA upregulated NLRP3 inflammasome components and damaged mitochondria.
  • NAC treatment improved cell viability and inhibited UA-induced NLRP3 inflammasome activation.
  • UA downregulated UCP2 expression.

Conclusions:

  • Soluble UA induces H9C2 cell damage through mitochondrial dysfunction and NLRP3 inflammasome activation.
  • Downregulation of UCP2 by UA contributes to cellular damage.
  • NAC exhibits protective effects against UA-induced cellular injury.
Keywords:
Myocardial cell damageNLRP3 inflammasomeSoluble uric acidUCP2

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