| Chronic cerebral hypoperfusion is chronic cerebrovascular in sufficiency for a long time because of all kinds of reasons. According to the epidemiological study, incidence of cerebrovascular disease is about 140-200/100000 population, average death rate is 100-200/100000 population. It brings out histopathological and biochemical changes in brain,which is a common pathological way in the period of many disease such as vascular dementia,Binswanger disease,Alzheimer disease .With the ratio of senile increasing in our country, prevention and treatment to diseases mainly from chronic cerebrovascular insufficiency is increasingl important. In the situation of cerebral hypoperfusion, pathological changes take place in nerve synapse, especially in cholinergic synapses. At the same time, free oxidate increases, SOD, its clearer, discreases, LPO increases with its toxic output-MDA increasingrelatively. MDA is a kind of to xicm atter, which can overoxidate cell membrane. Astrocytes increased, GFAP, their symbol protein, increased too.The main compent of HLF is Flavone mixture of crataegus leaves .It was reported that the total flavonoids have obvious efficiency on reducing blood press ,protectcting cradrac muscle with meagre blood and controlling blood platelet agglomerating. Furthermore, they have potent effects on antiaging, anticancer and can enhance organism immunity.The research indicates that total flavonoids can improve cerebrovascular cycle, improve energy metabolism, clear free oxidate, protect the intact of structure and ability of the cell membrane. Therefore ,it protects the neurons in hypoperfusion .Our study discussed the therapeutic mechanism of HLF through setting up cerebral ischemia- reperfusion model in rats by blocking middle cerebral artery,. In this project, we take the molecular technology to explore the mechanism to its neuroprotective effects. We made ischemia reperfusionmodel in rats to study the effects of HLF on neurocyte morphology changes and neurological scale.As the result of that the changes of neurocytes morphology are those ,neurons were serious edema cytoplasma was stained slightly and nucler were contracted and strained deeply after reperfusion. HLF (60mg/kg,30 mg/kg)reduced cellular edema,maintained the neurocyte morphology.After reperfusion,modle rats have distinct action deficits.Some rats flexed and adducted the left limbs,some rats rotated to the left side when it crawled,some rats were unconscious and could not crawl. HLF (60mg/kg,30 mg/kg)can reduced neurological scores(P﹤0.05),behavior deficits were dereased by HLF.The therapeutics efects of HLF were investigated in middle cerebral (MCAO) induced focal cerebral ischemi ribsion injury in rats. Male Sprague-Dawley rats were subjected to 4 h right MCAO via the intraluminal filament technique and 72h reperfusion. In this study, the neurological deficit score, infarct size,cerebral water content, brain malondialdehyde (MDA) content and antioxidant enzymes activities were measured. HLF (60mg/kg,30 mg/kg) significantly reduced the infarct size and water content,and produced significant in neurological deficits. HLF (60mg/kg,30 mg/kg) significantly inhibited theincreases of brain MDA content and prevented the activities of brain superoxide dismutase (SOD) and from declines caused cerebral ischemia-reperfusion (P<0.01). All these findings suggest that HLF has the therapeutic potential against focal ischemia-reperfusion injuryin rats. Therapeutics efects may be related to inhibition of lipidpe xidation, protection modulation of endogenous antioxidant enzyme activities.
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