Carbon monoxide (CO)
poisoning causes
cardiotoxicity and so far, no definite
antidote has been proposed to overcome CO-induced adverse outcomes.
Hesperidin, a citrus
flavonoid, has shown cardio-protective effects in cardiac
ischemia/reperfusion models. This study investigated the protective effects of
hesperidin against CO-induced cardiac injury. To induce CO
poisoning, rats were exposed to CO at 3000 ppm for 60 min. On the exposure day and the four following days,
hesperidin (at three different doses of 25, 50, and 100 mg/kg/day) was administered intraperitoneally. A group of animals received
normal saline and served as the control group. The electrocardiogram (ECG) was recorded and evaluated with special focus on S-T segment changes (depression or elevation), T-wave alterations,
AV block and ventricular and supraventricular arrhythmias. On day 6 (i.e., the day after the last injection day), the animals were sacrificed and the hearts were harvested and evaluated for
necrosis using
hematoxylin and
eosin staining. In addition, Akt
protein expression levels and BAX/BCL2 ratio were determined by western blotting. Our results showed that
hesperidin decreased cardiac
necrosis. In animals treated with
hesperidin 100 mg/kg, Akt
protein expression was increased, while the BAX/BCL2 ratio was significantly decreased. ECG changes were reversed in all groups 2 h following CO exposure, regardless of
hesperidin administration. Overall,
hesperidin decreased the deleterious cardiac effects of CO
poisoning in rats.