本文選題：蛛網(wǎng)膜下腔出血 + 細(xì)胞因子信號(hào)轉(zhuǎn)導(dǎo)負(fù)調(diào)控因子3�。� 參考：《南京大學(xué)》2014年碩士論文

【摘要】：研究背景及目的 蛛網(wǎng)膜下腔出血(SAH)是一種嚴(yán)重的神經(jīng)外科疾病。蛛網(wǎng)膜下腔出血后早期腦損傷(EBI)在遲發(fā)性腦缺血的發(fā)生發(fā)展中起到重要作用,并且是造成患者高致殘率及致死率的首要原因。蛛網(wǎng)膜下腔出血后早期腦組織發(fā)生氧化應(yīng)激、免疫炎癥反應(yīng)、細(xì)胞凋亡等病理生理改變。JAK/STAT信號(hào)通路參與多種信號(hào)通路級(jí)聯(lián)反應(yīng),細(xì)胞因子信號(hào)轉(zhuǎn)導(dǎo)負(fù)調(diào)控因子3(SOCS3)通過(guò)JAK/STAT通路調(diào)節(jié)信號(hào)傳導(dǎo)。由此考慮在蛛網(wǎng)膜下腔出血后的早期腦損傷,SOCS3參與其生理病理過(guò)程,并發(fā)揮調(diào)節(jié)信號(hào)轉(zhuǎn)導(dǎo)作用。本實(shí)驗(yàn)研究在蛛網(wǎng)膜下腔出血(SAH)后早期腦組織中SOCS3的分布和表達(dá)變化,及與炎性細(xì)胞因子相關(guān)性。方法成年雄性SD大鼠72只(250-300g,南京軍區(qū)總醫(yī)院動(dòng)物中心提供),分為對(duì)照組、SAH后3h、 6h、12h、24h、 48h、72h、5d、7d共9組(每組8只)。采用視交叉池注血法建立大鼠SAH模型,于SAH后不同時(shí)間點(diǎn)處死后取腦,應(yīng)用免疫印跡和免疫組化技術(shù)檢測(cè)SAH后腦組織中SCS3的分布和表達(dá)變化,并通過(guò)實(shí)時(shí)熒光定量聚合酶鏈反應(yīng)(Realtime-PCR)檢測(cè)炎性因子IL-1β及TNF-α表達(dá)及變化。結(jié)果SAH后大鼠腦組織中3h時(shí)SOCS3蛋白水平開(kāi)始升高,24h達(dá)到高峰,其后逐漸下降,7d仍高于對(duì)照組。SOCS3廣泛存在于神經(jīng)系統(tǒng)細(xì)胞中,其中神經(jīng)元與部分膠質(zhì)細(xì)胞均有較明顯SOCS3陽(yáng)性表達(dá)。同時(shí),對(duì)照組中SOCS 3主要定位于胞核,SAH后SOCS3胞漿陽(yáng)性增加,24h達(dá)到高峰,其后胞核胞漿陽(yáng)性都下降。Realtime-PCR示SAH后炎性介質(zhì)IL-1β表達(dá)顯著增加,3h后開(kāi)始升高,1d達(dá)第一個(gè)高峰,5d達(dá)到表達(dá)的第二個(gè)高峰,CNF-α于3h達(dá)到峰值,后逐漸減少。結(jié)論大鼠SAH后早期伴有SOCS3信號(hào)通路的激活,提示SOCS3信號(hào)通路參與SAH后早期腦損傷中的病理生理改變。炎性因子IL-1β及TNF-a參與大鼠SAH后腦損傷生理病理過(guò)程,可能通過(guò)SOCS3發(fā)揮作用。
[Abstract]:Background and objective Subarachnoid hemorrhage (SAH) is a serious neurosurgical disease. Early brain injury (EBI) after subarachnoid hemorrhage plays an important role in the occurrence and development of delayed cerebral ischemia and is the primary cause of high disability rate and fatality rate. Oxidative stress, immune inflammation, apoptosis and other pathophysiological changes in early brain tissue after subarachnoid hemorrhage. Cytokine signal transduction negative regulator 3 (SOCS 3) regulates signal transduction through JAK/STAT pathway. It is considered that early brain injury after subarachnoid hemorrhage may participate in the physiological and pathological process of SOCS3 and play a role in regulating signal transduction. The present study was designed to investigate the distribution and expression of SOCS3 in brain tissue after subarachnoid hemorrhage (SAH) and its correlation with inflammatory cytokines. Methods Seventy-two adult male Sprague-Dawley rats were divided into 9 groups (n = 8 in each group). They were divided into 9 groups (n = 8 in each group), which were provided by the Animal Center of Nanjing military region General Hospital for 3 h, 6 h, 12 h, 24 h, 48 h, 72 h, 5 d and 7 d after SAH respectively. The rat SAH model was established by injecting blood into the cistern of optic chiasma. The brain was killed at different time points after SAH. The distribution and expression of SCS3 in brain tissue after SAH were detected by immunoblotting and immunohistochemistry. The expression and change of inflammatory factor IL-1 尾 and TNF- 偽 were detected by real-time fluorescence quantitative polymerase chain reaction (PCR). Results the level of SOCS3 protein began to increase at 3 h after SAH and reached its peak at 24 h, and then decreased gradually at 7 days, which was still higher than that in the control group. SOCS3 was widely expressed in nervous system cells, and the positive expression of SOCS3 in neurons and some glial cells was obvious. At the same time, in the control group, SOCS 3 was mainly located in the nucleus of the cell, and the increase of SOCS3 cytoplasmic positive rate reached its peak at 24 h. After that, the expression of IL-1 尾 in the cytoplasm decreased. Realtime-PCR showed that the expression of IL-1 尾 in the inflammatory mediators increased significantly after SAH for 3 h, and the expression of IL-1 尾 began to increase at 1 day and reached the first peak at 5 days. The second peak of CNF- 偽 reached its peak at 3 h, and then decreased gradually. Conclusion the activation of SOCS3 signal pathway after SAH in rats suggests that SOCS3 signaling pathway is involved in the pathophysiological changes of early brain injury after SAH. Inflammatory factors IL-1 尾 and TNF-a participate in the physiological and pathological process of brain injury after SAH in rats, which may play a role through SOCS3.
【學(xué)位授予單位】：南京大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類(lèi)號(hào)】：R743.35

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