Tripartite motif protein 32 overexpression promotes inflammation and pyroptosis in INS-1 cells via the NF-κB/NLRP3 signaling pathway under high glucose conditions.

Authors

Tingting Wan, Hongjie Wang, Chunxu Wang, Yidan Wang, Xiudan Li, Yanbo Li

Published in

Endokrynologia Polska. Volume 77. Issue 5. Pages 528-536.

Abstract

β-cell dysfunction and insulin resistance are hallmarks of type 2 diabetes mellitus (T2DM), in which inflammation and pyroptosisare critically involved. Tripartite motif protein 32 (TRIM32) participates in inflammation and programmed cell death, but its role inβ-cell dysfunction remains unclear. This study investigated the role of TRIM32 in inflammation and pyroptosis in rat insulinoma (INS-1) cells.
INS-1 cells were cultured under high-glucose conditions. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to determine TRIM32 gene expression. Western blot analysis was performed to examine the expression of proteins associatedwith inflammation and pyroptosis. TUNEL staining and lactate dehydrogenase (LDH) release assays were performed to quantify celldeath. Rescue experiments were conducted to verify the findings.
TRIM32 overexpression promoted inflammation and pyroptosis in INS-1 cells under high-glucose conditions, whereas TRIM32 silencing had the opposite effects. In addition, BAY 11-7082 blocked the NF-κB/NLRP3 signaling pathway and significantly attenuated inflammation and pyroptosis in INS-1 cells under high-glucose conditions.
TRIM32 overexpression promoted inflammation and pyroptosis in INS-1 cells partly through the NF-κB/NLRP3 signaling pathway under high-glucose conditions.

PMID:
42949011
Bibliographic data and abstract were imported from PubMed on 28 Oct 2026.

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