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  本文關鍵詞： 實驗性自身免疫性腦脊髓炎 載脂蛋白E 水通道蛋白4 膠質纖維酸性蛋白　出處：《廣西醫(yī)科大學》2015年碩士論文　論文類型：學位論文

【摘要】：目的研究載脂蛋白E (ApoE)對實驗性自身免疫性腦脊髓炎(EAE)模型小鼠病灶中的星形膠質細胞的影響。方法采用髓鞘少突膠質細胞糖蛋白多肽35-55 (MOG35-55)作為抗原,分別誘導敲除ApoE基因的C57BL/6小鼠(ApoE-/-)及野生型(WT)C57BL/6J小鼠,建立EAE模型,對應設立E-ApoE-/-組和E-WT組。將野生型C57BL/6J小鼠注射等量生理鹽水以代替MOG35-55,設立正常對照組(C-WT)。免疫后第0-35天,每天上午由同一人對小鼠進行神經(jīng)功能缺損評分,并同時記錄。免疫后第35天,取各組小鼠的大腦和脊髓做石蠟切片,行HE染色,觀察各組小鼠腦組織中炎性細胞的浸潤情況。免疫組織化學染色法檢測各組小鼠的大腦和脊髓中水通道蛋白4(AQP4)與膠質纖維酸性蛋白(GFAP)的表達情況。結果E-ApoE-/-組和E-WT組于免疫后第11天相繼發(fā)病,發(fā)病率達100%。C-WT組無小鼠發(fā)病,活動度正常。兩組EAE小鼠的神經(jīng)功能缺損癥狀隨時間的延長而逐漸加重。與E-WT組小鼠比較,E-ApoE-/-組小鼠的神經(jīng)功能缺損評分峰值顯著升高(P0.05)；同時,E-ApoE-/-組小鼠的大腦和脊髓中浸潤的炎性細胞顯著多于E-WT組；與正常對照組小鼠相比,E-ApoE-/-組小鼠和E-WT組小鼠的大腦和脊髓中AQP4、GFAP的表達量均顯著升高(P均0.05)；另外,E-ApoE-/-組小鼠的大腦和脊髓中AQP4、GFAP的表達量均顯著高于E-WT組(P均0.05)。結論EAE小鼠中存在炎性浸潤以及星形膠質細胞水腫和增生,而ApoE的缺乏可以加重這些病理改變,ApoE可以作為MS防治的新的切入點,為MS的防治提供新的方向和理論參考。
[Abstract]:Objective to study the apolipoprotein E (ApoE) on experimental autoimmune encephalomyelitis (EAE) effects of lesions in a mouse model of astrocytes. Methods using myelin oligodendrocyte glycoprotein 35-55 (MOG35-55) as antigen, were induced in ApoE knockout mice (C57BL/6 ApoE-/-) and wild type (WT) C57BL/6J mice, EAE model is established, corresponding to the establishment of E-ApoE-/- group and E-WT group. The wild type C57BL/6J mice were injected with normal saline instead of MOG35-55, a normal control group (C-WT). 0-35 days after immunization, every morning by the same person on mouse nerve function deficit score was recorded at the same time, and thirty-fifth days. After immunization, the brain and spinal cord of mice were taken and paraffin sections were stained with HE, observed the infiltration of inflammatory cells in the brain tissue of mice. Immunohistochemical staining in the mice brain and spinal cord through the water Protein 4 (AQP4) and glial fibrillary acidic protein (GFAP). The expression results of E-ApoE-/- group and E-WT group on the eleventh day after immunization after onset, the incidence rate of 100%.C-WT group activity. Normal incidence of mice, prolong the neurological symptoms of EAE mice in two groups with time gradually increased. Compared with the mice in group E-WT, the neurological deficit scores significantly increased the peak in E-ApoE-/- group (P0.05); at the same time, the infiltration of inflammatory cells of the brain and spinal cord of mice in E-ApoE-/- group was significantly higher than in group E-WT; compared with normal control mice, AQP4 brain and spinal cord of mice in E-ApoE-/- group and E-WT group of mice, the expression of GFAP increased significantly (P < 0.05); in addition, AQP4 brain and spinal cord of mice in E-ApoE-/- group, the expression of GFAP was significantly higher than that of group E-WT (P < 0.05). There are inflammatory infiltration and astrocyte edema and the conclusion of EAE in mice The lack of ApoE can aggravate these pathological changes, and ApoE can be used as a new entry point for the prevention and control of MS, which provides a new direction and theoretical reference for the prevention and control of MS.

【學位授予單位】：廣西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：R744.51

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相關期刊論文 前1條

1 鄭明華;唐玉蘭;韋俊杰;梁培霄;陶敏;韋云飛;;載脂蛋白E擬肽對實驗性自身免疫性腦脊髓炎小鼠腦脊髓CD4~+、CD8~+ T淋巴細胞表達的影響[J];臨床神經(jīng)病學雜志;2013年03期

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本文編號：1443316