本文選題：一氧化碳中毒遲發(fā)性腦病 + SD大鼠��； 參考：《重慶醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的本課題通過(guò)建立一氧化碳中毒遲發(fā)性腦病SD大鼠動(dòng)物模型,研究一氧化碳中毒遲發(fā)性腦病腦組織表達(dá)的差異蛋白質(zhì),篩選出敏感性高、特異性強(qiáng)、具有診斷意義的差異蛋白質(zhì),從而為一氧化碳中毒遲發(fā)性腦病的病理機(jī)制、預(yù)防、早期診斷和藥物靶點(diǎn)治療等提供理論依據(jù)與參考。方法采用靜態(tài)染毒法建立一氧化碳中毒遲發(fā)性腦病SD大鼠模型并采用Morris水迷宮實(shí)驗(yàn)驗(yàn)證模型建立成功;提取腦組織進(jìn)行組織病理學(xué)檢查;運(yùn)用iTRAQ技術(shù)研究一氧化碳中毒遲發(fā)性腦病差異蛋白質(zhì)表達(dá)。結(jié)果成功建立了SD大鼠一氧化碳中毒遲發(fā)性腦病模型。染毒前、染毒后1d、3d、5d,對(duì)照組與CO染毒組平均潛伏期差異無(wú)統(tǒng)計(jì)學(xué)意義(p0.05);染毒后7d、11d、14d、19d,CO染毒組平均潛伏期時(shí)間明顯長(zhǎng)于對(duì)照組,差異具有統(tǒng)計(jì)學(xué)意義(p0.05)。組織病理學(xué)觀察發(fā)現(xiàn)CO染毒1天后,個(gè)別海馬錐體細(xì)胞變小,細(xì)胞核固縮、深染,結(jié)構(gòu)不清;CO染毒3天后,錐體細(xì)胞層變薄,錐體細(xì)胞數(shù)目減少,殘存錐體細(xì)胞變小,細(xì)胞核固縮、深染不清;CO染毒7、21、28天后,上述病理改變程度加重。運(yùn)用iTRAQ技術(shù)研究一氧化碳中毒遲發(fā)性腦病差異蛋白質(zhì)表達(dá),結(jié)果示染毒組與對(duì)照組蛋白質(zhì)共179個(gè)蛋白質(zhì)存在顯著差異;其中髓鞘脂蛋白、線粒體磷酸載體蛋白、鈣網(wǎng)膜蛋白、波形蛋白差異尤為明顯。結(jié)論本課題基于iTRAQ技術(shù)研究一氧化碳中毒遲發(fā)性腦病差異蛋白質(zhì)表達(dá),結(jié)果顯示兩者蛋白質(zhì)存在明顯差異,進(jìn)一步篩選特異性強(qiáng)的蛋白質(zhì),為一氧化碳中毒遲發(fā)性腦病的病理機(jī)制、預(yù)防、早期診斷和藥物靶點(diǎn)治療等提供理論依據(jù)與參考。
[Abstract]:Objective to study the differential protein expression in the brain tissue of delayed encephalopathy induced by carbon monoxide poisoning by establishing a SD rat model of delayed encephalopathy with carbon monoxide poisoning, and to screen out the differential protein with high sensitivity, specificity and diagnostic significance, which is the pathological mechanism of the delayed encephalopathy of carbon oxide poisoning, prevention and early prevention. The diagnosis and drug target treatment were provided with theoretical basis and reference. Methods the SD rat model of delayed encephalopathy with carbon monoxide poisoning was established by static poisoning and the model of Morris water maze test was used to establish the model successfully; the brain tissue was collected for histopathological examination, and the difference of delayed encephalopathy caused by carbon monoxide poisoning was studied by iTRAQ technique. Results the model of delayed encephalopathy of carbon monoxide poisoning in SD rats was successfully established. Before exposure, 1D, 3D, 5D, the average latency difference between the control group and the CO group was not statistically significant (P0.05); the average latency time of 7D, 11d, 14d, 19d, CO Dyeing Group was significantly longer than that of the control group, and the difference was statistically significant (P0.05). The pathological observation found that the pyramidal cells in the hippocampal pyramidal cells became smaller after 1 days of CO exposure, and the nucleus retraction, deep staining and unclear structure were found. After 3 days of exposure, the pyramidal cell layer became thinner, the number of pyramidal cells decreased, the remaining pyramidal cells became smaller, the nuclei were contracted and dyed deep; the above pathological changes were aggravated by the 7,21,28 after CO poisoning. ITRAQ technology research was used. The protein expression of delayed encephalopathy in carbon monoxide poisoning was investigated. The results showed that there were significant differences in 179 proteins between the 179 proteins in the infected group and the control group, and the difference of the sphingolipin, the mitochondrial phosphate carrier protein, the calamentin, and the vimentin was particularly obvious. Conclusion this lesson is based on the iTRAQ technique to study the delayed brain poisoning of carbon monoxide poisoning. The protein expression of the disease differentially shows that there is a significant difference in protein and further screening specific protein to provide theoretical basis and reference for the pathological mechanism, prevention, early diagnosis and drug target treatment of delayed encephalopathy with carbon monoxide poisoning.

【學(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R595.1;R747.9

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