本文選題：坐骨神經(jīng)　切入點(diǎn)：斷后　出處：《汕頭大學(xué)》2005年碩士論文　論文類型：學(xué)位論文

【摘要】：背景 組織纖溶酶原激活物(tissue plasminogen actiVator,tPA) 是一種具有蛋白溶解活性的絲氨酸蛋白,它一直被臨床用作腦栓塞急性 期治療的藥物。但隨著近年來(lái)研究的深入,發(fā)現(xiàn)tPA不僅具有溶栓的作 用,而且它在神經(jīng)元損傷時(shí)還可促使神經(jīng)元死亡。另有一些證據(jù)表明 tPA有調(diào)節(jié)小膠質(zhì)細(xì)胞活化和促進(jìn)神經(jīng)元凋亡的雙重作用。由于小膠 質(zhì)細(xì)胞數(shù)量的增加和tPA濃度的高低相平行,tPA完全可被作為小膠質(zhì) 細(xì)胞增殖的一個(gè)指標(biāo)。Ca~(2+)內(nèi)流是引起tPA釋放的主要因素,因此推 測(cè)在坐骨神經(jīng)離斷后即在神經(jīng)元軸突橫斷的情況下,神經(jīng)元發(fā)生強(qiáng)烈的 電活動(dòng),導(dǎo)致Ca~(2+)內(nèi)流,先是受損的神經(jīng)元釋放少量的tPA來(lái)激活病變 部位的小膠質(zhì)細(xì)胞,這些活化的小膠質(zhì)細(xì)胞再釋放大量的tPA,一方面 促使自身的增殖活化,另一方面當(dāng)tPA超過(guò)神經(jīng)元的致死濃度時(shí),便引 起了神經(jīng)元的死亡。近年來(lái)在對(duì)tPA的研究中,人們大多是在中樞神 經(jīng)系統(tǒng)(central nervous system,CNS)損傷后來(lái)觀察tPA的作用,這往 往造成CNS中血管通透性的改變,血液中的tPA釋放到CNS中,干擾 實(shí)驗(yàn)結(jié)果.因此我們選擇坐骨神經(jīng)作為研究對(duì)象,在只造成坐骨神 經(jīng)損傷的前提下對(duì)tPA在脊髓中的作用進(jìn)行初步研究。同時(shí)周圍神經(jīng)損 傷后再生研究的重點(diǎn)已從局部的外科修復(fù),發(fā)展到采用多因子多因素防 止神經(jīng)元胞體、神經(jīng)纖維、效應(yīng)器的變性,保護(hù)神經(jīng)損傷后神經(jīng)元,減 少不可逆損傷的發(fā)生,綜合有效地促進(jìn)神經(jīng)的再生。本課題的完成將為
[Abstract]:Background tissue plasminogen activator (plasminogen). Is a serine protein with proteolytic activity, which has been used clinically for acute cerebral embolism. But with the development of research in recent years, it is found that tPA not only has thrombolytic effect. It can also promote neuronal death in the event of neuronal injury. There is also some evidence that. TPA can regulate the activation of microglia and promote neuronal apoptosis. The increase of the number of cytoplasm cells parallel to the concentration of tPA can be used as microglia. An indicator of cell proliferation. Caan2) influx is the main factor causing tPA release. In the case of neuronal axon transection after sciatic nerve dissection, the neurons developed intense. Electrical activity, resulting in Ca~(2) inward flow, first damaged neurons release a small amount of tPA to activate the lesion. Microglia in the site, these activated microglia release a large amount of tPA, on the one hand, Promote self proliferation and activation, on the other hand, when tPA exceeds the lethal concentration of neurons, it causes. The death of neurons. In recent years, in the study of tPA, people are mostly in the central nervous system. To observe the role of tPA after central nervous damage. Causing changes in vascular permeability in CNS, releasing tPA from blood into CNS, interfering. So we chose the sciatic nerve as the object of study. The role of tPA in spinal cord was studied on the premise of injury. The focus of posttraumatic regeneration research has evolved from local surgical repair to multifactorial and multifactorial prevention. Degeneration of neuronal bodies, nerve fibers, and effectors, protection of neurons after nerve injury, reduction of neurons. The occurrence of less irreversible damage and the comprehensive and effective promotion of nerve regeneration. The completion of this project will be
【學(xué)位授予單位】：汕頭大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2005
【分類號(hào)】：R361

【引證文獻(xiàn)】

相關(guān)碩士學(xué)位論文 前1條

1 張勇;周圍神經(jīng)阻滯麻醉對(duì)脊髓生物學(xué)影響的實(shí)驗(yàn)研究[D];新疆醫(yī)科大學(xué);2008年

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本文編號(hào)：1596132