Abstract
Recent studies suggest that dietary virgin olive oil (VOO) reduces hypoxia-reoxygenation injury in rat brain slices. We sought to extend these observations in an in vivo study of rat cerebral ischemia-reperfusion injury. Four groups, each consisting of 18 Wistar rats, were studied. One group (control) received saline, while three treatment groups received oral VOO (0.25, 0.5, and 0.75 mL/kg/day, respectively). After 30 days, blood lipid profiles were determined, before a 60-min period of middle cerebral artery occlusion (MCAO). After 24-h reperfusion, neurological deficit scores, infarct volume, brain edema, and blood brain barrier permeability were each assessed in subgroups of six animals drawn from each main group. VOO reduced the LDL/HDL ratio in doses of 0.25, 0.5, and 0.75 mL/kg/day in comparison to the control group (p < 0.05), and offered cerebroprotection from ischemia-reperfusion. For controls vs. doses of 0.25 vs. 0.5 vs. 0.75 mL/kg/day, attenuated corrected infarct volumes were 207.82 ± 34.29 vs. 206.41 ± 26.23 vs. 124.21 ± 14.73 vs. 108.46 ± 31.63 mm3; brain water content of the infarcted hemisphere was 82 ±± 0.25 vs. 81.5 ± 0.56 vs. 80.5 ± 0.22 vs. 80.5 ± 0.34%; and blood brain barrier permeability of the infarcted hemisphere was 11.31 ± 2.67 vs. 9.21 ± 2.28 vs. 5.83 ± 1.6 vs. 4.43 ± 0.93 µg/g tissue (p < 0.05 for measures in doses 0.5 and 0.75 mL/kg/day vs. controls). Oral administration of VOO reduces infarct volume, brain edema, blood brain barrier permeability, and improves neurologic deficit scores after transient MCAO in rats.
Highlights
Brain ischemia induces the release of excitatory amino acids, with subsequent receptor activation leading to calcium influx, metabolic and electrophysiological dysfunction, and oxidative stress
We sought to characterize the impact of dietary virgin olive oil (VOO) on brain infarct volume, brain edema, blood brain barrier permeability, and neurological dysfunction resulting from transient middle cerebral artery occlusion (MCAO) in rats
Our data suggest that pretreatment with dietary VOO may reduce infarct volume, brain edema, blood brain barrier (BBB) permeability, and neurobehavioral deficit scores in a reliable and reproducible animal model of stroke followed by reperfusion[11]
Summary
Brain ischemia induces the release of excitatory amino acids, with subsequent receptor activation leading to calcium influx, metabolic and electrophysiological dysfunction, and oxidative stress TheScientificWorldJOURNAL (2010) 10, 1180–1191 peroxidation)[1] Subsequent reperfusion worsens this oxidative stress, potentiating ischemic injury[2]. A key component of this diet is olive oil, which contains monounsaturated fatty acids (MUFA) and polyphenols, compounds with a clear antioxidant effect[5]. Tyrosol has neuroprotective effects in a model of transient focal cerebral ischemia in rats[8], and both HT and HT acetate protect brain slices subjected to hypoxia-reoxygenation[9]. While past studies suggest that virgin olive oil (VOO) may protect brain slices from oxidative stress[9,10], in vivo neuroprotective effects from ischemia-reperfusion injury have yet to be clarified. We sought to characterize the impact of dietary VOO on brain infarct volume, brain edema, blood brain barrier permeability, and neurological dysfunction resulting from transient middle cerebral artery occlusion (MCAO) in rats
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