[Effect of dietary olive leaf extract on brain cholesterol, cholesterol ester and triglyceride levels and of brain edema in rat stroke model]

Brain injury by transient complete global brain ischemia [cardiac arrest] and regional incomplete brain ischemia [ischemic stroke] afflicts a very large number of patients with death or permanent disability. Recent studies suggest that olive extracts suppress inflammation and reduce stress oxidative injury. The aim of the study was to evaluate the effect of dietary Olive Leaf Extract [OLE] on brain cholesterol, cholesterol ester and triglyceride levels as well as brain edema in rat stroke model. 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 [MCAO]-operated [n=6] and intact subgroups [n=6] for assessment of neuropathology [brain edema] and brain lipid analysis. The brain cholesterol, cholesterol ester and triglyceride levels were greater in experimental groups when compared to controls. Olive leaf extracts reduced brain edema in experimental groups of 75 and 100 mg/kg/day. Our data suggest that OLE may be cerebroprotective in a rat model of ischemia-reperfusion. Further work is required to extend these observations

Prolonged oral administration of oleuropein might protect heart against aconitine-induced arrhythmia

In this study, it was surveyed to know whether an oral single dose of oleuropein could mimic the cardiac preconditioning in rats' hearts or whether its prolonged oral administration could protect the heart against the aconitine-induced arrhythmia in rats. Eighty male Wistar rats were divided into two series [n = 8 in each group]. In the first series, all groups [except the control [Con] group] were given a single oral dose of oleuropein [20 mg/Kg] 1, 3, 24 and 48 h before the infusion of aconitine. In the second series, except the Con group, the other four groups were given oral oleuropein [20 mg/Kg/day] for 3, 7, 14 and 28 days, before the infusion of aconitine. Electrocardiogram was recorded to monitor arrhythmia. Data of the first series showed that the initiation time of arrhythmia, the initiation of ventricular tachycardia [VT], the numbers of reversible ventricular fibrillation [VF] and the death time had no significant difference compared with Con group. In the second series, a significant protection was occurred only in the 28 days group that was evident with increased initiation time of arrhythmia, increased initiation time of VT, and increased the number of reversible VF and death time in compared to the Con group. The findings of this study show that the oral administration of a single dose of oleuropein could not mimic the preconditioning effects in rat hearts, but the prolonged administration of oleuropein for about four weeks could protect the heart against aconitine-induced arrhythmia

[ effect of various doses of olive leaf extract on brain lipid levels and blood brain barrier permeability in rat stroke model]

Recent studies suggest that olive extract can suppress inflammation and reduce stress oxidative injury. We sought to extend these observations in an in vivo study of rat cerebral ischemia-reperfusion injury. In this experimental study, five groups, each consisting of 12 male Wistar rats, were studied. First group [control] received distilled water, while three treatment groups received oral olive leaf extract [OLE] for 30 days [50, 75 and 100 mg/kg/day, respectively]. The last group [sham] underwent surgery without ischemia and did not receive OLE. Two hours after the last dose, each group was subdivided into two subgroups. In the first subgroup middle cerebral artery occlusion [MCAO] was induced during an operation, in order to assess neuropathology [blood brain barrier permeability], while the second subgroup remained intact and was used for brain lipid analysis. The brain cholesterol levels in 50, 75, and 100 mg/kg/day OLE group were 34.4 +/- 4.7, 35.9 +/- 5.8, and 38.3 +/- 2.1 mg/g brain tissue weight, respectively; the cholesterol ester levels in them were 15.2 +/- 1.8, 15.8 +/- 3.1 and 16.3 +/- 3.6 mg/g brain tissue weight, respectively. These numbers were greater than the controls. Brain triglyceride levels in the 50 mg/kg/day group were similar to that in controls; but it was higher in the 75 and 100 mg/kg/day groups [34.1 +/- 0.5 And 34.5 +/- 1.1 mg/g brain tissue weight, respectively]. The OLE reduced blood brain barrier permeability in 75 and 100 mg/kg/day group when compared to controls [p< 0.000, p< 0.000, respectively]. There was significant difference between right and left hemisphere in control group and 50 mg/kg/day group [p< 0.000]. Our data suggest that OLE reduced the blood brain barrier permeability and changed brain lipids which may be cerebroprotective in a rat model of ischemia-reperfusion. Further work is required to extend these observations