Tri Astiawati, Mohammad Saifur Rohman, Titin Wihastuti, Hidayat Sujuti, Agustina Endharti, Djanggan Sargowo, Delvac Oceandy, Bayu Lestari, Efta Triastuti, Ricardo Adrian Nugraha
While the beneficial effects of colchicine on inflammation and infarcted myocardium have been documented, its impact on cardiac fibroblast activation in the context of myocardial infarction (MI) remains unknown. This study aimed to investigate the effect of colchicine on the regulation of NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation and Interleukin-1β (IL-1β) expression in fibroblasts. 3T3 fibroblasts were exposed to 600 μM CoCl2 for 24 h to simulate hypoxia, with normoxic cells as controls. Colchicine (1 μM) was administered for 24 h. ASC-NLRP3 colocalization and IL-1β expression were evaluated using immunofluorescence and flow cytometry, respectively. Data were analyzed using t-tests and one-way ANOVA with post hoc tests. Hypoxia treatment significantly induced apoptosis-associated speck-like protein containing a CARD (ASC)-NLRP3 colocalization (p < 0.05). Colchicine treatment of hypoxic 3T3 cells reduced ASC-NLRP3 colocalization, although this reduction was not statistically significant. Additionally, IL-1β expression was significantly inhibited in colchicine-treated hypoxic 3T3 cells compared to those treated with placebo (p < 0.05). The findings of this study indicate that colchicine treatment inhibits the activation of the NLRP3 inflammasome by disrupting the colocalization of ASC and NLRP3, thereby reducing IL-1β expression in CoCl2-treated 3T3 cells. © 2025 by the authors.
Doctoral Program of Medical Science, Faculty of Medicine, Brawijaya University, Malang, 65145, Indonesia; Department of Cardiology, Doctor Iskak General Hospital, Tulungagung, 62233, Indonesia; Department of Cardiology and Cardiovascular Medicine, Faculty of Medicine, Brawijaya University, Malang, 65145, Indonesia; Cardiovascular Research Centre, Brawijaya University, Malang, 65145, Indonesia; Department of Biomedical, Nursing Science, Faculty of Medicine, Brawijaya University, Malang, 65145, Indonesia; Department of Biochemistry, Faculty of Medicine, Brawijaya University, Malang, 65145, Indonesia; Department of Cardiology and Vascular Medicine, Faculty of Medicine, Brawijaya University, Malang, 65145, Indonesia; Division of Cardiovascular Science, The University of Manchester, Manchester Academic Health Science Centre, Manchester, M13 9PT, United Kingdom; Department of Pharmacology, The University of Manchester, Manchester Academic Health Science Centre, Manchester, M13 9PT, United Kingdom; Department of Pharmacy, Faculty of Medicine, Brawijaya University, Malang, 65145, Indonesia; Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Airlangga—Dr, Soetomo General Academic Hospital, Surabaya, 60286, Indonesia
