Colchicine attenuates myocardial inflammation, endothelial dysfunction, and apoptosis in a rat model of alcohol-related cardiac damage

Chronic alcohol consumption is a recognized contributor to non-ischemic dilated cardiomyopathy, particularly in individuals with an underlying genetic predisposition, through myocardial inflammation, oxidative stress, and apoptosis. Colchicine, an NLRP3 inflammasome inhibitor, has cardioprotective potential, but its role in alcohol-induced injury is unknown. This study aimed to evaluate the dose-dependent effects of colchicine (0.1 mg/kg and 0.3 mg/kg) on alcohol-induced cardiac damage in rats.

Overall, 40 Sprague-Dawley rats were randomized into five groups: control, alcohol (20% ethanol, 2.5 g/kg i.p.), colchicine alone, alcohol + standard-dose colchicine, and alcohol + high-dose colchicine. After 28 days, blood, cardiac, and liver tissues were analyzed for oxidative stress, inflammation, vascular injury, and apoptosis markers, along with histopathology.

Alcohol exposure significantly increased oxidative stress, inflammatory (interleukin-1β, tumor necrosis factor α, high-sensitivity C‑reactive protein), vascular injury, and apoptotic markers (all p < 0.001). Colchicine attenuated these elevations dose-dependently, with the high dose (0.3 mg/kg) providing significantly greater protection across nearly all parameters (p < 0.001). Histopathology confirmed that colchicine reduced alcohol-induced cardiomyocyte hypertrophy and inflammatory infiltration.

Colchicine exerts dose-dependent cardioprotective effects against alcohol-induced injury by mitigating inflammation, oxidative stress, and apoptosis. High-dose colchicine offers superior protection, suggesting its potential therapeutic role in alcohol-related cardiac damage.