Background and Objectives. Neuroprotection agents may help improve the outcomes of large vessel ischemic stroke. This study aims to explore the role of Virgin Coconut Oil (VCO), with its well-documented anti-oxidant properties, in neuroprotection after transient occlusion of the extracranial internal carotid artery in a rat model of stroke. Methods. Twenty-three Sprague-Dawley rats were randomized into two groups: 1) control group (n=11) given distilled water, and 2) treatment group (n=12) given virgin coconut oil at 5.15 ml/kg body weight for seven days. Subsequently, the rats underwent transient right extracranial internal carotid artery occlusion (EICAO) for 5 minutes using non-traumatic aneurysm clips. At 4 and 24 hours after EICAO, the animals were examined for neurologic deficits by an observer blinded to treatment groups, then sacrificed. Eight brain specimens (4 from each group) were subjected to histopathologic examination (H & E staining) while the rest of the specimens were processed using triphenyltetrazolium chloride (TTC) staining to determine infarct size and area of hemispheric edema. Results. VCO treatment significantly improved the severity of neurologic deficit (1.42 ± 2.31) compared to the control distilled water group (4.09 ± 2.59) 24 hours after EICAO. Whereas, infarct size and percent hemispheric edema did not significantly differ between the two groups. Conclusion. Prophylactic treatment of VCO is protective against EICAO-induced neurologic deficits in a rat model. VCO shows great potential as a neuroprotective agent for large vessel ischemic stroke. However, more studies are necessary to elucidate the neuroprotective mechanisms of VCO therapy in ischemic stroke.
Coconut Oil ; Oxidants ; Antioxidants ; Neuroprotection ; Ischemia ; Stroke