Cardioprotective effects of gallic acid in a rat ischemia-reperfusion model: role of apoptosis, inflammation, and antioxidant defense.

Background and purpose: Heart disease is a major global health problem. Gallic acid (GA) possesses cardioprotective properties. This study aimed to evaluate the therapeutic effects of GA pretreatment in ischemia-reperfusion (I/R) and elucidate its underlying mechanisms. Experimental approach: Forty adult male Wistar rats were subjected to this experiment. GA was given to the rats through gavage at doses of 15 and 30 mg/kg/day, 10 days before the induction of ischemia. To induce I/R, the left anterior descending coronary artery was occluded for 30 min, and reperfusion continued for 24 h. Malondialdehyde (MDA) levels, antioxidant enzyme activity, and inflammatory cytokines were assessed using kits. Myocardial injury markers were analyzed by ELISA, and infarct size was assessed through 2,3,5-triphenyltetrazolium chloride staining. Real-time polymerase chain reaction was utilized to quantify the relative gene expression of Bax and Bcl-2. Findings/Results: The findings indicated that pretreatment with GA led to significant improvement in inflammatory cytokines, antioxidant enzyme activity, and a decrease in MDA levels. GA also decreased infarct size and myocardial injury markers significantly. Moreover, pretreatment with GA revealed a significant increase in the expression of the Bcl-2 gene, while the expression of the Bax gene decreased. Conclusion and implications: Inclusively, the results suggested that GA may hold significant potential as a therapeutic agent for reducing myocardial injury in the context of I/R, with 30 mg/kg/day proving more effective than 15 mg/kg/day, offering a promising path for further investigation.