Intravenous Administration of Coenzyme Q10 in Acute Period of Cerebral Ischemia Decreases Mortality by Reducing Brain Necrosis and Limiting Its Increase within 4 Days in Rat Stroke Model

Abstract

Oxidative stress plays a key role in the pathogenesis of ischemic stroke. Coenzyme Q10 has a multi-targeting effect and may protect the brain against ischemic damage. The aim of our study was to evaluate the neuroprotective potential of ubiquinol by its intravenous administration. The study was performed on rats; a stroke was modeled by occlusion of the middle cerebral artery. On days 1 and 4 after ischemia, the neurological deficit and volume of the brain lesion were determined by MRI and TTC staining. Intravenous administration of coenzyme Q10 led to a decrease in rat mortality rate, improvement in neurological status, and decrease in the brain necrosis area in acute and delayed period after cerebral ischemia. A single intravenous administration of ubiquinol led to a limitation of the size of the brain damage for at least four days after ischemia. Thus, intravenous administration of coenzyme Q10 has a persistent neuroprotective potential. This finding suggests a possible therapeutic role of ubiquinol in acute ischemic conditions.

Keywords

• coenzyme Q10
• ubiquinol
• ubiquinone
• brain ischemia
• neuroprotection
• stroke