實(shí)驗(yàn)性大鼠彌漫性腦損傷后GFAP、NO和ET的變化研究
發(fā)布時(shí)間：2018-10-10 11:12
【摘要】：背景和目的 創(chuàng)傷性腦損傷(Traumatic brain injury，TBI)有較高發(fā)生率，是導(dǎo)致創(chuàng)傷病人傷殘及死亡的主要原因，嚴(yán)重危害人類健康，給社會(huì)和家庭帶來沉重負(fù)擔(dān)。彌漫性腦損傷(Diffuse brain injury，DBI)在TBI中占有重要地位，流行病學(xué)調(diào)查顯示DBI占交通傷后重型腦創(chuàng)傷的73％。長(zhǎng)期以來，DBI被認(rèn)為是腦損傷后持續(xù)性昏迷及嚴(yán)重神經(jīng)功能障礙的主要原因，有人統(tǒng)計(jì)創(chuàng)傷性昏迷病人資料發(fā)現(xiàn)有55％重度腦創(chuàng)傷病人存在DBI。DBI后可誘發(fā)系列病理生理改變(如腦血管自主調(diào)節(jié)功能紊亂、血腦屏障通透增加、腦組織缺血、顱內(nèi)壓增高等)、腦組織各種物質(zhì)(如氧自由基、鈣離子、興奮性氨基酸、炎性細(xì)胞因子、電解質(zhì)等)代謝紊亂及細(xì)胞凋亡等，造成腦組織繼發(fā)損害，進(jìn)一步加重病人腦損傷程度。目前對(duì)DBI的研究逐漸深入，但其機(jī)理尚未完全闡明，限制了治療學(xué)的發(fā)展。研究DBI發(fā)病機(jī)制及其傷后病理生理變化、探索行之有效的腦保護(hù)治療途徑，將有助于提高病人的生存率及生存質(zhì)量。我們改進(jìn)了Marmarou法制作大鼠彌漫性腦損傷模型，，利用該模型觀察損傷后腦組織的病理變化，檢測(cè)反應(yīng)性星形細(xì)胞(astrocyte，Ast)膠質(zhì)纖維酸性蛋白(glial fibrillary acidic protein，GFAP)表達(dá)變化，并研究一氧化氮(nitric oxide，NO)和內(nèi)皮素(endothlin，ET)在大鼠創(chuàng)傷腦組織中不同時(shí)間含量的變化規(guī)律，以探討顱腦損傷的病理機(jī)制，進(jìn)一步闡明三者在顱腦損傷后病理生理變化中的作用，為臨床治療腦損傷提供實(shí)驗(yàn)基礎(chǔ)。 方法 1、建立彌漫性腦損傷動(dòng)物模型：采用Marmarou方法改良制作大鼠DBI模型。同時(shí)建立對(duì)照組進(jìn)行對(duì)照比較。
[Abstract]:Background and objective traumatic brain injury (Traumatic brain injury,TBI) has a high incidence and is the main cause of disability and death of traumatic brain injury patients, which seriously endangers human health. It puts a heavy burden on society and families. Diffuse brain injury (Diffuse brain injury,DBI) plays an important role in TBI. Epidemiological investigation shows that DBI accounts for 73% of severe brain injury after traffic injury. DBI has long been considered to be the main cause of persistent coma and severe neurological dysfunction after brain injury. Some statistics showed that 55% of the patients with severe brain trauma had DBI.DBI, which could induce a series of pathophysiological changes (such as cerebral vascular autonomic regulatory dysfunction, increased blood-brain barrier permeability, cerebral ischemia. Various substances (such as oxygen free radicals, calcium ions, excitatory amino acids, inflammatory cytokines, electrolytes, etc.) metabolic disorders and apoptosis, etc. The degree of brain injury was further aggravated. At present, the research on DBI has gradually deepened, but its mechanism has not been fully elucidated, which limits the development of therapeutics. To study the pathogenesis of DBI and its pathophysiological changes after injury and to explore an effective way of brain protection therapy will help to improve the survival rate and quality of life of patients. We improved the Marmarou method to make the model of diffuse brain injury in rats. The pathological changes of brain tissue and the expression of glial fibrillary acidic protein (glial fibrillary acidic protein,GFAP) in reactive astrocytes (astrocyte,Ast) were observed by using the model. The changes of the contents of nitric oxide (nitric oxide,NO) and endothelin (endothlin,ET) in traumatic brain tissue of rats at different time were studied in order to explore the pathophysiological mechanism of traumatic brain injury and to elucidate the role of them in the pathophysiological changes after traumatic brain injury. To provide experimental basis for clinical treatment of brain injury. Methods 1. The animal model of diffuse brain injury was established. Marmarou method was used to improve the DBI model of rats. At the same time, the control group was established for comparison.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：R361
本文編號(hào)：2261545
[Abstract]:Background and objective traumatic brain injury (Traumatic brain injury,TBI) has a high incidence and is the main cause of disability and death of traumatic brain injury patients, which seriously endangers human health. It puts a heavy burden on society and families. Diffuse brain injury (Diffuse brain injury,DBI) plays an important role in TBI. Epidemiological investigation shows that DBI accounts for 73% of severe brain injury after traffic injury. DBI has long been considered to be the main cause of persistent coma and severe neurological dysfunction after brain injury. Some statistics showed that 55% of the patients with severe brain trauma had DBI.DBI, which could induce a series of pathophysiological changes (such as cerebral vascular autonomic regulatory dysfunction, increased blood-brain barrier permeability, cerebral ischemia. Various substances (such as oxygen free radicals, calcium ions, excitatory amino acids, inflammatory cytokines, electrolytes, etc.) metabolic disorders and apoptosis, etc. The degree of brain injury was further aggravated. At present, the research on DBI has gradually deepened, but its mechanism has not been fully elucidated, which limits the development of therapeutics. To study the pathogenesis of DBI and its pathophysiological changes after injury and to explore an effective way of brain protection therapy will help to improve the survival rate and quality of life of patients. We improved the Marmarou method to make the model of diffuse brain injury in rats. The pathological changes of brain tissue and the expression of glial fibrillary acidic protein (glial fibrillary acidic protein,GFAP) in reactive astrocytes (astrocyte,Ast) were observed by using the model. The changes of the contents of nitric oxide (nitric oxide,NO) and endothelin (endothlin,ET) in traumatic brain tissue of rats at different time were studied in order to explore the pathophysiological mechanism of traumatic brain injury and to elucidate the role of them in the pathophysiological changes after traumatic brain injury. To provide experimental basis for clinical treatment of brain injury. Methods 1. The animal model of diffuse brain injury was established. Marmarou method was used to improve the DBI model of rats. At the same time, the control group was established for comparison.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：R361
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