| Chronic cerebral hypoperfusion is chronic cerebrovascular insufficiency for a long time because of all kinds of reasons. Accordingto the epidemiological study, incidence of cerebrovasculardisease is about 140-200/100000 population, average death rate is100-200/100000 population. It brings out histopathological andbiochemical changes in brain,which is a common pathological way in theperiod 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 chroniccerebrovascular insufficiency is increasingl important. In thesituation of cerebral hypoperfusion, pathological changes take place innerve synapse, especially in cholinergic synapses. At the same time, freeoxidate increases, SOD, its clearer, discreases, LPO increases with itstoxic output-MDA increasingrelatively. MDA is a kind of to xicm atter,which can overoxidate cell membrane. Astrocytes increased, GFAP, theirsymbol protein, increased too.It was reported that the total flavonoidshave obvious efficiency on reducing blood press ,protectcting cradracmuscle with meagre blood and controlling blood platelet agglomerating.Furthermore, they have potent effects on antiaging, anticancer and canenhance organism immunity.The research indicates that total flavonoids can improvecerebrovascular 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 protect mechanism of HLF through nextexperimental animal models. In this project, we take the moleculartechnology to explore the mechanism to its neuroprotective effects. inour study,rats cerebral ischemia reperfusion injury was induced bymiddle cerebral artery occlusion.The neurological out come wasevaluated.CK,LDH and NO activity in serum,SOD and MDA levels ofcerebral tissue were measured.Blood stasis model is created by injectionadrenamine and codness stimulation to investigate the effects of HLF onblood viscosity,thrombus and platelet aggregation rate and to explorethe mechanism.We made ischemia reperfusion model in rats to study the effects ofHLF on neurocyte morphology changes and neurological scale.As the resultof that the changes of neurocytes morphology are those ,neurons wereserious edema cytoplasma was stained slightly and nucler were contractedand strained deeply after reperfusion.HLF(60mg/kg,30 mg/kg)reducedcellular edema,maintained the neurocyte morphology.Afterreperfusion,modle rats have distinct action deficits.Some rats flexedand adducted the left limbs,some rats rotated to the left side when itcrawled,some rats were unconscious and could not crawl.HLF(60mg/kg,30 mg/kg)can reduced neurological scores(P﹤0.05),behavior deficitswere dereased by HLF.The protective efects of HLF were investigated in middle cerebral(MCAO) induced focal cerebral ischemi ribsion injury in rats. MaleSprague-Dawley rats were subjected to 2 h right MCAO via the intraluminalfilament technique and 22 h reperfusion. In this study, the neurologicaldeficit score, infarct size,cerebral water content, brainmalondialdehyde (MDA) content and antioxidant enzymes activities weremeasured. HLF(60mg/kg,30 mg/kg) significantly reduced the infarct sizeand water content,and produced significant in neurological deficits.HLF(60mg/kg,30 mg/kg) significantly inhibited theincreases of brain MDAcontent and prevented the activities of brain superoxide dismutase (SOD)and from declines caused cerebral ischemia-reperfusion (P<0.01). Allthese findings suggest that HLF has the protective potential againstfocal ischemia-reperfusion injuryin rats. Protective efects may berelated to inhibition of lipidpe xidation, protection modulation ofendogenous antioxidant enzyme activities.To study the effects of HLF on thrombus formation and plateletaggregation.Thrombus formation was assessed by electricity stimulateinduced thrombosis in artery in rats.We found that HLF(60mg/kg,30mg/kg)could prolong thrombosed time(P﹤0.01,P﹤0.05).The effect of YXTon thrombus in vitro, HLF(60mg/kg,30 mg/kg)could shorten the length ofthrombus significantly.HLF(60mg/kg)could also decrease wet weight anddry weight of thrombus, HLF(30 mg/kg)only decrease wet weight ofthrombus.We also study the effect of platelet aggregation induced by ADPin rats,we found HLF(60mg/kg,30 mg/kg) inhabited platelet aggregationin vitro induce by ADP.Study of mechanism of improvement in rat,s brain ischemia injuriesIn there groups, HLF can notable decrease the possibility of plateletadhesiveness, it is a big difference which the contrast group (P<0.05,p< 0.01).HLF can refrain platelet congregation, there are evidentdecrease in rate of platelet congregation (P<0.05,P<0.01,P<0.001).It can release the brain edema which the ischemia-induced braindamage reduce. It can release the injury of ischemia of fat overoxidizing.It can increase the activity of SOD in the brain tissue, andcan prohibit. So it has the function of releasing free radical formation,contending with fat over oxidizing and protecting brain nerve.
|
PDF Full Text Request