【摘要】：大量研究表明缺氧是造成神經(jīng)元死亡的重要原因之一，宮內(nèi)缺氧可致胎兒宮內(nèi)窘迫而損傷腦細(xì)胞，造成生長發(fā)育遲緩，同時因累及神經(jīng)系統(tǒng)發(fā)育中的多個區(qū)域而遺留永久性的損傷，成活者常遺留腦癱、智力低下等嚴(yán)重后遺癥。腦源性神經(jīng)營養(yǎng)因子(brain-derived neurotrophic factor，BDNF)作為腦組織中含量最豐富的神經(jīng)營養(yǎng)因子，，在中樞神經(jīng)系統(tǒng)內(nèi)合成并廣泛存在于腦組織，包括大腦皮層、海馬、基底前腦、紋狀體、下丘腦和小腦，其中以海馬和皮層中含量最高。BDNF通過其特異性受體酪氨酸激酶(TrkB)參與細(xì)胞的分化、粘著、增殖與成熟等重要的生物學(xué)過程。目前已有大量研究表明，在腦外傷、低血糖、腦缺血、腦缺氧及抽搐損傷時，細(xì)胞內(nèi)BDNF其受體TrkB的表達(dá)均受到明顯影響，加入外源性BDNF可有效減輕神經(jīng)元所受損傷。 我們前期已用多種試驗方法證明了BDNF對缺氧胚鼠腦皮質(zhì)神經(jīng)元有確切保護(hù)作用，但BDNF與TrKB結(jié)合后將胞外刺激信號傳遞入核內(nèi)的機制尚未完全明確。BDNF細(xì)胞內(nèi)信號傳遞途徑主要有兩條，即絲裂原活化蛋白激酶(Mitogen-activated protein kinase，MAPK)信號通路和磷酯酰肌醇3激酶(phosphatidylinositol-3-kinase，PI-3-K)／AKT信號通路。在
[Abstract]:A large number of studies have shown that hypoxia is one of the important causes of neuron death. Intrauterine hypoxia can cause fetal distress and damage brain cells, resulting in growth retardation. At the same time, permanent damage is left over from multiple areas of nervous system development. Survivors often leave serious sequelae such as cerebral palsy, mental retardation and so on. As the most abundant neurotrophic factor in brain tissue, brain-derived neurotrophic factor (brain-derived neurotrophic factor,BDNF) is synthesized and widely distributed in the central nervous system, including cerebral cortex, hippocampus, basal forebrain and striatum. The hypothalamus and cerebellum have the highest content in hippocampus and cortex. BDNF participates in the important biological processes of cell differentiation adhesion proliferation and maturation through its specific receptor tyrosine kinase (TrkB). A large number of studies have shown that the expression of BDNF receptor TrkB in brain injury, hypoglycemia, cerebral ischemia, cerebral anoxia and convulsion injury is significantly affected. Exogenous BDNF can effectively alleviate the neuronal injury. We have demonstrated the protective effect of BDNF on cerebral cortical neurons in anoxic embryos by several experimental methods. However, the mechanism of extracellular stimulation signal transduction into nucleus after BDNF and TrKB binding is not completely clear. There are two main signal transduction pathways in BDNF cells, that is, mitogen-activated protein kinase (Mitogen-activated protein kinase,). MAPK signaling pathway and phosphoryl inositol 3 kinase (phosphatidylinositol-3-kinase,PI-3-K) / AKT signaling pathway. In
【學(xué)位授予單位】：四川大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2006
【分類號】：R363

【引證文獻(xiàn)】

相關(guān)碩士學(xué)位論文 前1條

1 劉書紅;鹽酸美金剛對血管性癡呆大鼠CREB和細(xì)胞色素C表達(dá)的影響[D];鄭州大學(xué);2010年

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