基于iTRAQ技术一氧化碳中毒迟发性脑病的蛋白质组学研究

发布时间：2018-04-23 05:25

本文选题：一氧化碳中毒迟发性脑病 + SD大鼠　；参考：《重庆医科大学》2017年硕士论文

【摘要】：目的本课题通过建立一氧化碳中毒迟发性脑病SD大鼠动物模型,研究一氧化碳中毒迟发性脑病脑组织表达的差异蛋白质,筛选出敏感性高、特异性强、具有诊断意义的差异蛋白质,从而为一氧化碳中毒迟发性脑病的病理机制、预防、早期诊断和药物靶点治疗等提供理论依据与参考。方法采用静态染毒法建立一氧化碳中毒迟发性脑病SD大鼠模型并采用Morris水迷宫实验验证模型建立成功;提取脑组织进行组织病理学检查;运用iTRAQ技术研究一氧化碳中毒迟发性脑病差异蛋白质表达。结果成功建立了SD大鼠一氧化碳中毒迟发性脑病模型。染毒前、染毒后1d、3d、5d,对照组与CO染毒组平均潜伏期差异无统计学意义(p0.05);染毒后7d、11d、14d、19d,CO染毒组平均潜伏期时间明显长于对照组,差异具有统计学意义(p0.05)。组织病理学观察发现CO染毒1天后,个别海马锥体细胞变小,细胞核固缩、深染,结构不清;CO染毒3天后,锥体细胞层变薄,锥体细胞数目减少,残存锥体细胞变小,细胞核固缩、深染不清;CO染毒7、21、28天后,上述病理改变程度加重。运用iTRAQ技术研究一氧化碳中毒迟发性脑病差异蛋白质表达,结果示染毒组与对照组蛋白质共179个蛋白质存在显著差异;其中髓鞘脂蛋白、线粒体磷酸载体蛋白、钙网膜蛋白、波形蛋白差异尤为明显。结论本课题基于iTRAQ技术研究一氧化碳中毒迟发性脑病差异蛋白质表达,结果显示两者蛋白质存在明显差异,进一步筛选特异性强的蛋白质,为一氧化碳中毒迟发性脑病的病理机制、预防、早期诊断和药物靶点治疗等提供理论依据与参考。
[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.

【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R595.1;R747.9

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