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Updated: Feb 23, 2026
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
Zinc inhibits high glucose-induced NLRP3 inflammasome activation in human peritoneal mesothelial cells
Yi Fan1, Xiuli Zhang1, Lina Yang1
1Department of Nephrology, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning 110001, P.R. China.
Abstract:
Zinc (Zn) deficiency is important for inducing nucleotide-binding domain and leucine‑rich repeat‑containing family, pyrin domain-containing-3 (NLRP3) inflammasome activation in macrophages. However, its function in the NLRP3 inflammasome activation of peritoneal mesothelial cells (PMCs) remains to be elucidated. In the present study, the human PMC (HPMC) line HMrSV5 was co‑treated with high glucose and either ZnSO4 or a Zn chelator. The activity of the NLRP3/caspase‑1 inflammasome was assessed via western blot analysis, immunofluorescence, reverse transcription‑quantitative polymerase chain reaction and ELISA. In addition, the activity of the nuclear factor erythroid 2‑related factor 2 (Nrf2) pathway was detected using western blotting, and the level of reactive oxygen species (ROS) was assessed by 2,7‑dichlorofluorescein fluorescence and flow cytometry. It was found that Zn supplementation inhibited HG‑induced NLRP3 inflammasome activation in the HPMCs by attenuating ROS production. Further experiments revealed that Zn supplementation inhibited the HG‑induced production of ROS through activation of the Nrf2 antioxidant pathway. These results indicated that Zn inhibited NLRP3 inflammasome activation in the HG‑treated HPMCs by activating the Nrf2 antioxidant pathway and reducing the production of ROS.
Insights
Zinc supplementation inhibits high glucose-induced NLRP3 inflammasome activation in human peritoneal mesothelial cells. This occurs by activating the Nrf2 antioxidant pathway, which reduces reactive oxygen species (ROS) production.
Area of Science:
- Cell Biology
- Immunology
- Metabolism
Background:
- Zinc deficiency is known to activate the NLRP3 inflammasome in macrophages.
- The role of zinc in NLRP3 inflammasome activation within peritoneal mesothelial cells (PMCs) is not well understood.
- High glucose conditions can impact cellular functions and inflammatory responses.
Purpose of the Study:
- To investigate the effect of zinc on high glucose-induced NLRP3 inflammasome activation in human PMCs (HPMCs).
- To elucidate the underlying mechanisms involving reactive oxygen species (ROS) and the Nrf2 pathway.
Main Methods:
- Human PMC (HMrSV5) cells were treated with high glucose and either zinc sulfate or a zinc chelator.
- NLRP3/caspase-1 inflammasome activity was assessed using western blot, immunofluorescence, RT-qPCR, and ELISA.
- Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway activity and ROS levels were measured via western blotting and flow cytometry.
Main Results:
- Zinc supplementation significantly inhibited high glucose-induced NLRP3 inflammasome activation in HPMCs.
- Zinc attenuated the production of reactive oxygen species (ROS) in high glucose-treated HPMCs.
- Zinc activated the Nrf2 antioxidant pathway, which mediated the reduction in ROS production.
Conclusions:
- Zinc plays a protective role against high glucose-induced NLRP3 inflammasome activation in HPMCs.
- The mechanism involves the activation of the Nrf2 antioxidant pathway, leading to decreased ROS levels.
- These findings highlight the potential of zinc in managing cellular inflammation under high glucose conditions.
