The aim of the present study was to evaluate the efficiency of combination of hyperbaric oxygen (HBO) and an antioxidant on permanent focal cerebral ischemia. Male Wistar rats underwent permanent middle cerebral artery occlusion (MCAO). Then, animals were randomly assigned to one of four groups: the control group (n=9) received no treatment, HBO group (n=9) was treated for 90 min at 2.5 absolute atmosphere for 3 days, the U-74389G group (n=8) received single U-74389G injection (3 mg/kg), the HBO + U-74389G group (n=8 ) received both HBO and U-74389G treatments. Treatments were initiated within the first 10 min after MCAO. After 3 days, the infarct volumes in rat brains were measured. The infarct ratios were 25.6±6.5 % for the control group, 21.9±6.4 % for the HBO group, 15.7±5.7 % for U-74389G group and 12.5±3.8 % for HBO + U74389G group. The infarct volumes were significantly reduced in rats treated with U-74389G (p< 0.05) and combination therapy (p <0.05). HBO failed to reduce infarct volume significantly. We concluded that 1) U-74389G is more beneficial than HBO on permanent MCAO in rats, and 2) a combined therapy failed to significantly improve infarct volume more than either single treatment., G. Acka, A. Sen, Z. Canakci, S. Yildiz, A. Akin, G. Uzun, H. Cermik, I. Yildirim, S. Kokpinar., and Obsahuje bibliografii a bibliografické odkazy
Ongoing interest in brain ischemia research has provided data showing that ischemia may be involved in the pathogenesis of Alzheimer disease. Brain ischemia in the rat produces a stereotyped pattern of selectiv e neuronal degeneration, which mimics early Alzheimer disease pathology. The objective of this study was to further develop an d characterize cardiac arrest model in rats, which provides practical way to analyze Alzheimer- type neurodegeneration. Rats were made ischemic by cardiac arrest. Blood-brain barrier (BBB) insufficiency, accumulation of different parts of amyloid precursor protein (APP) and platelets inside and outside BBB vessels were investigated in ischemic brain up to 1-year survival. Isch emic brain tissue demonstrated haphazard BBB changes. Toxic fr agments of APP deposits were associated with the BBB vessels. Moreover our study revealed platelet aggregates in- and outside BBB vessels. Toxic parts of APP and platelet aggregates correlated very well with BBB permeability. Progressive injury of the ischemic brain parenchyma may be caused not only by a degeneration of neurons destroyed during ischemia but also by chronic damage in BBB. Chronic ischemic BBB insufficiency with accumulation of toxic components of APP in the brain tissue perivascular space, may gradually over a lifetime, progress to brain atrophy and to full blown Alzheimer-type pathology., M. Jabłoński., and Obsahuje bibliografii a bibliografické odkazy
Neuroprotective effects of estrogens and progesterone have been widely studied in various experimental models. The present study was designed to compare possible neuroprotective effects of 17alpha-estradiol, 17beta-estradiol, and progesterone on oxidative stress in rats subjecte d to global cerebral ischemia. Global cerebral ischemia was induced in ovariectomized female rats by four vessel occlusion for 10 min. Following 72 h of reperfusion, levels of malondialdehyde (MDA, oxidative stress marker), and reduced glutathione (GSH, major endogenous antioxidant) were assessed in hippocampus, striatum and cortex of rats treated with either 17alpha-estradiol, 17beta-estradiol, progesterone or estradiol + progesterone beforehand. Steroid administration ameliorated ischemia-induced decrease in GSH and increase in MDA levels. Our data offers additional evidence that estrogens and progesterone or combination of two exert a remarkable neuroprotective effect reducing oxidative stress., V. H. Ozacmak, H. Sayan., and Obsahuje seznam literatury