Lauric acid mitigates doxorubicin-induced cardiotoxicity in rats: Modulation of oxidative stress and inflammation via NF-?B p65 attenuation

Background: Cardiotoxic effects of doxorubicin (DOX) have been reported in cancer patients, which mainly stem from the production of reactive oxygen species (ROS). This oxidative damage contributes to myocardial injury, inflammation, and altered cardiac function. Lauric acid (LA) is a medium-chain saturated fatty acid present in coconut oil and is known for its antioxidant properties, making it a potential cardioprotective candidate against DOX-induced toxicity. Objectives: The present study was conducted to evaluate the cardioprotective effects of LA in a DOX-induced cardiotoxicity model by assessing biochemical, hematological, oxidative stress, histological, and molecular parameters in Wistar rats. Methods: Wistar rats were divided into four groups (n = 6): control (Tween 20), LA (500 mg/kg), DOX (15 mg/kg) and LA + DOX groups. The rats were sacrificed and evaluated for hematological indices, lipid profile and cardiac biomarkers, including CK-MB, cardiac troponin I (cTnI) and LDH. Cardiac tissue was analyzed for MDA, CAT, SOD, histopathological assessment, gene expression (NF-?B p65, IL-6 and TNF-?) and cytokine levels (IL-6 and TNF-?) after the 14-day study period. Additional comparative evaluation between DOX and LA + DOX groups was performed to determine the extent of cardioprotection. Results: The DOX reduced the body weight of rats, dysregulated hematological and lipid profiles and upregulated cardiac markers in serum. It also increased MDA levels, depleted CAT and SOD levels, altered cardiac cell histoarchitecture and elevated the gene and protein expressions of the cytokines. LA mitigated DOX-mediated cardiotoxicity by reducing oxidative stress and inflammation. LA also improved biochemical values, preserved myocardial structure and restored the antioxidant status compared to the DOX group. Conclusion: In conclusion, LA treatment protects the cardiac tissue against DOX-induced cardiotoxicity, as evidenced by its antioxidant and anti-inflammatory potential, supporting its possible therapeutic role.