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Atorvastatin Reduces Alcohol-Related Cardiac and Liver Tissue Damage, Oxidative Stress, Inflammation, Apoptosis, and
Cumaali Demirtas1, Şahhan Kılıç2, Mert Babaoğlu3
1Hamidiye Health Sciences Institute, University of Health Sciences, Istanbul, Turkiye.
Abstract:
Excessive alcohol consumption causes significant cardio-hepatic damage. This study investigated the effects of standard (10 mg/kg) and high (40 mg/kg) doses of atorvastatin on fibrosis, hypertrophy, apoptosis, inflammation, oxidative stress, mitochondrial-mediated apoptotic pathways, and thiol/disulfide balance in alcohol-induced heart and liver injury. Forty Sprague-Dawley rats were divided into five groups (n = 8; 4 male/4 female): Control (CONT), ALCOHOL (2.5 g/kg 20% ethanol i.p./28 days), ATOR (10 mg/kg o.g./28 days), ALCOHOL + ATOR (10 mg/kg o.g./28 days) and ALCOHOL+ hATOR (40 mg/kg o.g./28 days). Histopathologically, alcohol caused cardiac myocyte dilation, vacuolization, inflammation, and hepatic cord disruption. While standard ATOR partially improved tissue architecture (p < 0.001), the ALCOHOL+ hATOR group showed the lowest severity. Alcohol exposure significantly increased apoptosis (Caspase-3, M30, M65), oxidative stress (TOS, OSI, MDA), ischemia (IMA), and inflammatory cytokines (IL-1β, TNF-α, HsCRP, Endothelin-1) across serum, heart, and liver samples, while decreasing TAS, total thiol, and native thiol levels (p < 0.001 for all vs. CONT). Conversely, high-dose atorvastatin (ALCOHOL + hATOR) significantly reversed alcohol-induced toxicity by decreasing Caspase-3, M30, M65, TOS, OSI, MDA, TNF-α, HsCRP, Endothelin-1, and disulfide levels, while significantly restoring TAS, total thiol, and native thiol levels (p < 0.001 vs. ALCOHOL). TAS was significantly higher in the ALCOHOL+hATOR group than the ALCOHOL + ATOR group (p < 0.001). Despite marked improvements by hATOR, OSI, TOS, IL-1β, and HsCRP levels remained higher than CONT (p < 0.001). High-dose atorvastatin (40 mg/kg) exerts robust pleiotropic, anti-apoptotic, and antioxidant cytoprotection. By preserving thiol-disulfide homeostasis and limiting inflammation, high-dose atorvastatin effectively mitigates alcohol-induced subchronic cardiac and hepatic injury.
