Evaluation of the Neuroprotective Effects of Idebenone in an Experimental Carbon Monoxide Poisoning Model

Carbon monoxide (CO) poisoning is among the main causes of poisoning-related mortality and morbidity, primarily affecting the central nervous system and leading to delayed neurological sequelae. Idebenone exerts antioxidant and neuroprotective effects. In this study, we aimed to evaluate the specific neuroprotective effects of idebenone against CO poisoning. Forty female Wistar Albino rats were used in this study. Except the controls, the other rats inhaled 5000 ppm CO until a change in consciousness was observed. Rats with carboxyhemoglobin concentrations over 20% in blood samples collected from the tail vein were considered successful acute CO poisoning models. The rats were divided into five groups: healthy control (HC; group 1), CO + saline (CO-S; group 2), CO + 100 mg/kg idebenone (CO-I100; group 3), CO + 200 mg/kg idebenone (CO-I200; group 4), and CO + 300 mg/kg idebenone (CO-I300; group 5). Pre-determined doses of idebenon were orally administered to the rats at 24-h intervals for 5 days. The rats were anesthetized and sacrificed 24 h after the last drug dose. Histopathological and biochemical parameters were examined in the blood and hippocampus samples of the rats. Histopathological grading of neurons in the hippocampus revealed that the CO-S group exhibited the highest number of grade 1, 2, and 3 degenerative cells (all p = 0.001). Apoptotic index was the highest in the CO-S group and significantly low in the idebenone-treated groups (p = 0.001). Neuron-specific enolase and malondialdehyde levels and oxidative stress index were significantly lower in both the hippocampus and serum samples of the idebenone-treated groups than in those of the CO-S group (all p values = 0.001). Overall, idebenone inhibited degeneration due to CO-induced brain damage and exerted neuroprotective effects against oxidative stress in rats.