Antifibrotic effects of colchicine on 3T3 cell line ischemia to mitigate detrimental remodeling

Context: Acute myocardial infarction (AMI) is one of the clinical manifestations of coronary heart disease caused by the cessation of coronary blood flow. The development of the management of AMI has resulted in a reduction in the mortality rate of AMI patients. Nevertheless, the apparent inflammation triggers detrimental remodeling, so antifibrotic such as colchicine are needed. Aims: To analyze the impact of colchicine administration on the reduction of ventricular remodeling through the NLRP3 inflammasome, TGF-β, and α-SMA in a 3T3 cell line culture under ischemic conditions. Methods: The 3T3 cell line culture underwent ischemia treatment using CoCl2 and subsequent treatment with colchicine. This treatment was conducted for 24 hours with a concentration of 300 μM CoCl2, followed by the administration of colchicine at a concentration of 1 μM after the ischemia treatment. The expression levels of NLRP3, TGF-β, and α-SMA were assessed using flow cytometry, and the data were analyzed through one-way ANOVA. Results: Administration of colchicine for 24 hours following ischemia resulted in a significant decrease in the relative levels of NLRP3, TGF-β, and α-SMA (p<0.05) compared to the ischemia group. Conclusions: In vitro administration of colchicine can reduce post-ischemic remodeling, including the NLRP3 inflammasome, TGF-β, and α-SMA.