| Background and purpose: The appropriate methods of prevention and therapy for cerebral ischemia(CI) to restore the function of damaged neurons as well as to reduce disability and mortality remain a subject of debate. In middle-cerebral artery (MCA) stroke, physiologic imaging also allows pathophysiological differentiation into four tissue subtypes: i) already irreversibly damaged ("core"); ii) severely hypoperfused ("penumbra"); iii) mildly hypoperfused ("oligaemia"),; and iv) reperfused or hyperperfused. In the core ,the damaged neurons necrosis, but in the penumbra , the neurons indicate apoptosis. Saving the penumbra represents the main target of acute stroke therapy. Apoptosis is controlled by some genes, bcl-2 is a sort of anti-apoptosis and bax , on the contrary, is an auxo-apoptosis gene . The expressions of theose two genes are argued important factors to apoptosis. the brain drived neurotrophic fator(BDNF) who belongs to the neurotrophic factors (NTFs) plays an important role to maintain the function and even the regenration of neurons. Aspirin(ASA) is a non-steroidal anti-inflammatory drug with a wide spectrum of pharmacological activities and multiple sites of action. Apart from its preventive actions against stroke due to its antithrombotic properties, recent data in the literature suggest that ASA also exert direct neuroprotective effects. However it has not been reported whether ASA affect the apoptisics and the expression of BDNF. So, the aim of this study was mainly to investigate the possible effect of ASA might has on the neuron apoptisis and the expression of BDNF after reversible focal.ischemia. Methods:Established the rat MCA cerebral ischemia/reperfusion (CI/RP)model with suture occlusion technique according to modified Zea Longa method and then the rats were devide into four groups: one contrast group and there therapy groups with different dose of ASA(low dose: 20 mg·kg –1,middle dose: 80 mg·kg –1and large dose: 320 mg·kg –1) via an i.p. rote right after the CI/RP were performed and the next 2 days followed .After the CI/RP, the neurologic impairment evaluation score were recorded though a Bederson method for four days. The rats were then killed at the fouth day and some of the brains were removed to measure the infarct volume , the others were detected apoptosis by TUNEL technology and protein bcl-2, protein bax and BDNF levels by immunohistochemistry technology. Results:Neurologic impairment in various degree appeared in the contrast group rat after CI/RP.The infarct brain area, where showed white colour because not stained by TTC, can be distinguished clearly to the normal brain where showed red colour. TUNEL positive cell which can represented apoptosic neurons mainly appeared in the penum-bra. Propein Bcl-2 , Bax and BDNF can be determinated by immuno-histochemistry technology.Bcl-2 positive cells which concentrated highly in the penumbra appeared an relative normal shape with an completed nuclei ,on the contrary, Bax positive cells which concentrated near to the necrosis core appeared an fusiform shape with an shrinkaged nuclei.BDNF positive cells appeared in the whole ischemia area separately. When the ASA of different doses was i.p. to the rats in the there therapy groups , the results of every detection items described above changed as follows: the neurologic impairment lessened, the infarct volume reduced, the number of TUNEL positive cells decreased, the protein Bcl-2 expression increased as well as protein Bax expression reduced, the BDNF expression increased.Conlusion: 1.The application of ASA early after CI/RP can reduce infarct volume; 2.The application of ASA early after CI/RP can decrease neurologic impairment; 3.The application of ASA early after CI/RP can inhibit the neuron apoptosis of ischemic area via enhanced protein Bcl-2 expression as well as reduced protein Bax expression; 4. The application of ASA early after CI/RP can increase endogenous BDNF expression; 5.The effect of inhibition the neuron apoptosis and increase endogenous BDNF expressio...
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