BACKGROUND: Recent studies suggest that olive extracts suppress inflammation and reduce stress oxidative injury. We have attempted to determine the effect of dietary olive leaf extract (OLE) on brain lipidomics in rat stroke model. METHODS: Five groups, each consisting of 12 male Wistar rats, were studied. First and second groups (control, and sham) received distilled water, while three treatment groups received oral olive leaf extract (OLE) for 30 days (50, 75 and 100 mg/kg/day, respectively). Two hours after the last dose, each main group was subdivided to Middle cerebral artery occlusion-operated and intact subgroup for assessment of neuropathology (neurologic deficit scores and infarct volume), brain lipid analysis and brain glutathione levels, respectively. RESULTS: OLE increased the brain cholesterol ester, cholesterol, cerebroside and phosphatidylcholine levels in doses of 50, 75 and 100 mg/kg/day. OLE increased the brain triglyceride levels in doses of 75 and 100 mg/kg/day and OLE reduced the brain ceramide levels in doses of 50, 75 and 100 mg/kg/day in comparison to the control group (p<0.05). CONCLUSION: Although further studies are needed, it seems that the mechanism of OLE-induced ischemic tolerance in rats is partly associated with changes in brain lipids level.
BACKGROUND: Recent studies suggest that olive extracts suppress inflammation and reduce stress oxidative injury. We have attempted to determine the effect of dietary olive leaf extract (OLE) on brain lipidomics in ratstroke model. METHODS: Five groups, each consisting of 12 male Wistar rats, were studied. First and second groups (control, and sham) received distilled water, while three treatment groups received oral olive leaf extract (OLE) for 30 days (50, 75 and 100 mg/kg/day, respectively). Two hours after the last dose, each main group was subdivided to Middle cerebral artery occlusion-operated and intact subgroup for assessment of neuropathology (neurologic deficit scores and infarct volume), brain lipid analysis and brain glutathione levels, respectively. RESULTS: OLE increased the brain cholesterol ester, cholesterol, cerebroside and phosphatidylcholine levels in doses of 50, 75 and 100 mg/kg/day. OLE increased the brain triglyceride levels in doses of 75 and 100 mg/kg/day and OLE reduced the brain ceramide levels in doses of 50, 75 and 100 mg/kg/day in comparison to the control group (p<0.05). CONCLUSION: Although further studies are needed, it seems that the mechanism of OLE-induced ischemic tolerance in rats is partly associated with changes in brain lipids level.
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