This study aimed to investigate the potential neuroprotective effects of coenzyme Q10 in cerebral ischemia-reperfusion injury-induced neuronal damage and explore the underlying mechanisms. Twenty-eight adult male rats, weighing approximately 200-300 grams, were randomly divided into four groups: the sham group (neck dissection without ischemia), the control group (30 minutes of bilateral common carotid artery ligation followed by one hour of reperfusion), the vehicle group (oral carboxymethylcellulose solution for seven days prior to bilateral common carotid artery ligation and reperfusion), and the treatment group (seven days of coenzyme Q10 pretreatment followed by bilateral common carotid artery occlusion and reperfusion). Histopathological analysis and measurement of brain infarct size were performed, and cerebral levels of IL-6, IL-10, TNF-α, ICAM-1, NF-κB p65, and total antioxidant capacity were assessed. These cerebral tissue levels and cerebral infarct size were significantly elevated in the control and vehicle groups compared to the sham group. Conversely, the total antioxidant capacity was significantly reduced in these groups. Coenzyme Q10 treatment resulted in a significant increase in IL-10 and total antioxidant capacity levels, along with a significant decrease in IL-6, ICAM-1, TNF-α, and NF-κB p65 levels. Histopathological analysis revealed a significant reduction in ischemic damage in the coenzyme Q10-treated group. Coenzyme Q10 has neuroprotective properties in rats subjected to cerebral ischemia/reperfusion injury, possibly through its anti-inflammatory and anti-oxidative effects.
Keywords: CI/RI; Coenzyme Q10; ICAM-1; IL-10; IL-6; NF-κB p65; TNF-α; total anti-oxidant capacity.
© 2023 The Author(s).