ArticleInternational journal of molecular sciences2021
Acute Glucose Shift Induces the Activation of the NLRP3 Inflammasome in THP-1 Cells.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- [Immunometabolic disorders in type 2 diabetes mellitus mediated by NLRP3 inflammasome activation and methods of pharmacological correction thereof].Problemy endokrinologii · 2026Review
- When glycobiology meets inflammasome activation: Insights and implications.Journal of advanced research · 2026Review
- Serum Albumin and Glycemic Variability Could Contribute to Diabetic Retinopathy Progression by Regulating Chronic Inflammatory Pathways.Journal of ophthalmology · 2025Article
- Paeonol attenuated high glucose-induced apoptosis via up-regulating miR-223-3p in mouse cardiac microvascular endothelial cells.Scientific reports · 2024Article
- Diabetic Cardiomyopathy Uncovered: Transcriptomics, NLRP3, and Carvedilol Mechanisms.Journal of diabetes research · 2024Article
- Differences and Associations of NLRP3 Inflammasome Levels with Interleukins 1α, 1β, 33 and 37 in Adults with Prediabetes and Type 2 Diabetes Mellitus.Biomedicines · 2023Article
- The NLRP3-Inflammasome in Health and Disease.International journal of molecular sciences · 2022Article
- Diabetes Mellitus Promotes the Development of Atherosclerosis: The Role of NLRP3.Frontiers in immunology · 2022Review
- Anti-hyperglycemic contours of Madhugrit are robustly translated in theFrontiers in endocrinology · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We aimed to investigate the effect of acute glucose shift on the activation of the NLRP3 inflammasome, IL-1β secretion, and underlying signaling pathways in THP-1 cells. THP-1 cells were divided into four groups and exposed to the following glucose concentrations for 24 h: constant normal glucose (NG, 5.5 mM), constant high glucose (HG, 25 mM), normal to high glucose shift (NG-to-HG, 5.5 to 25 mM), and high to normal glucose shift (HG-to-NG, 25 to 5.5 mM). Cell viability, oxidative stress, and the levels of NLRP3 inflammasome components were assessed. Both directions of the acute glucose shift increased the activation of the NLRP3 inflammasome, generation of reactive oxygen species (ROS), and expression of phosphorylated p38 MAPK, JNK, and NF-κB compared with either constant NG or HG. Treatment with N-acetylcysteine, a pharmacological antioxidant, inhibited the acute glucose shift-induced generation of ROS, activation of NLRP3 inflammasome, and upregulation of MAPK-NF-κB. Further analysis using inhibitors of p38 MAPK, JNK, and NF-κB indicated that acute glucose shifts promoted IL-1β secretion by activating the signaling pathway in a ROS-MAPK-NF-κB-NLRP3 inflammasome in THP-1 cells. These findings suggested that acute changes in glucose concentration might cause monocyte inflammation, which is associated with diabetic complications.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.