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作 者:杨程程[1] 韦俊杰[2] 唐玉兰[1] 郑明华[1] 韦云飞[1]
机构地区:[1]广西医科大学第一附属医院神经内科,广西南宁530021 [2]广西壮族自治区人民医院神经内科,广西南宁530021
出 处:《中风与神经疾病杂志》2015年第1期33-36,共4页Journal of Apoplexy and Nervous Diseases
基 金:国家自然基金项目(项目批准号:81260188;81460194);广西自然科学基金资助项目(2012GXNSFAA053082);广西高等学校立项科研项目(201204LX050)
摘 要:目的探索载脂蛋白E(apolipoprotein E,apo E)对实验性自身免疫性脑脊髓炎(experimental autoimmune encephalomyelitis,EAE)模型小鼠病灶星形胶质细胞的影响。方法采用MOG35-55诱导apo E基因敲除的C57BL/6小鼠(apo E-/-EAE组)及野生型C57BL/6小鼠(普通EAE组),建立EAE模型。取免疫后35 d的EAE小鼠的大脑及脊髓切片,行HE染色,免疫组织化学染色法观察各组小鼠水通道蛋白4(AQP4)和胶质纤维酸性蛋白(GFAP)的表达。结果 apo E-/-EAE组和普通EAE组大脑和脊髓AQP4、GFAP的表达量均高于正常对照组,差异均有统计学意义(P<0.05);apo E-/-EAE组大脑和脊髓AQP4、GFAP表达量均高于普通EAE组,差异均有统计学意义(P<0.05)。结论 EAE中存在星形胶质细胞水肿、增生,apo E缺乏可以加重这一病变。Objective Abstract: Objective To explore the effect of apolipoprotein E on astrocyte cytotoxic edema and reactive astrogliosis in mice with experimental autoimmune encephalomyelitis. Methods 20 female C57 BL /6 mice were randomly divided into 2 groups. And the third group incuded 10 female apo E- /- mice on a C57 BL /6 background. EAE model was induced by immunized with myelin oligodendrocyte glycoprotein peptides( MOG35-55) in mice. The expression of AQP4 and GFAP was detected by immunohistochemistry. Results The expression of AQP4 and GFAP in the apo E- /- EAE group and common EAE group was more than the control group in brain( P 〈0. 05) and spinal cord( P 〈0. 05).More importantly,the expression of AQP4 and GFAP in the apo E- /- EAE group was beyond the common EAE group in brain( P 〈0. 05) and spinal cord( P 〈0. 05). Conclusion Apo E deficience may aggravate astrocyte cytotoxic edema and increase the formation of reactive astrogliosis in EAE.
关 键 词:载脂蛋白E 实验性自身免疫性脑脊髓炎 水通道蛋白4 胶质纤维酸性蛋白
分 类 号:R744[医药卫生—神经病学与精神病学]
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