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作 者:蒙晓珍 韦俊杰[2] 唐玉兰[1] 杨程程[3] 龚靖[1] 孙淑君[1]
机构地区:[1]广西医科大学第一附属医院神经内科,南宁市530021 [2]广西壮族自治区人民医院神经内科,南宁市530021 [3]广西中医药大学第一附属医院康复科,南宁市530023
出 处:《实用医学杂志》2016年第11期1738-1741,共4页The Journal of Practical Medicine
基 金:国家自然科学基金项目(编号:81260188,81460194);广西自然科学基金项目(编号:2012GXNSFAA053082,2015GXNSFAA139212);广西卫生厅自筹经费项目(编号:Z2012097)
摘 要:目的:探讨载脂蛋白E(Apo E)对脊髓切片培养模型中脂多糖(LPS)诱导的星形胶质细胞损伤的影响。方法:用振动切片机横向切取生后7 d大的C57BL/6 Apo E基因敲除型(Apo E-/-)及野生型(WT)小鼠脊髓切片进行培养,培养至第7天加入LPS共孵育5 d建立模型组(Apo E-/-LPS组、WT-LPS组),同时设立不加LPS的正常对照组。用免疫荧光检测脊髓片水通道蛋白-4(AQP4)、胶原纤维酸性蛋白(GFAP)及小胶质细胞标记物Iba1的表达,分别用ELISA和硝酸还原酶法测定培养液中TNF-α和NO的浓度。结果:模型组均出现AQP4和GFAP的表达缺失,即星形胶质细胞的损伤,且Apo E-/-LPS组的脊髓片损伤积分比WT-LPS组高(P<0.05);与正常对照组比较,模型组Iba1的表达及TNF-α、NO的浓度均升高(P<0.05),且Apo E-/-LPS组TNF-α和NO的浓度均高于WT-LPS组(P<0.05)。结论:Apo E缺乏加重星形胶质细胞的损伤,可能是通过促进小胶质细胞分泌促炎性介质而发挥作用。Objective To explore the effect of apolipoprotein E deficiency on astrocyte destruction in the ex vivo spinal cord slice model. Methods Vibratome-cut transverse spinal cord slices from C57BL/6 postnatal day 7 ApoE -/- mice and wild-type mice were euhured on transwell porous supports. After 7 days in the cuhure, spinal cord slices were exposed to LPS for 5 days. The expression of AQP4, GFAP and Ihal was detected by immunofluoreseence. The concentration of TNF-α and NO were detected by ELISA and method of nitrate reductase, respectively. Results Marked loss of AQP4 and GFAP staining were shown in LPS-affected groups, not in the control group, and the lesion score was higher in ApoE-/-group than WT-group (P 〈 0.05). In addition, the expression of Ibal and c, oncentration of TNF-α, NO in the LPS-affected groups were more than that of the control group (P 〈 0.05), and they were higher in the ApoE-/-LPS group than the WT-LPS group (P 〈 0.05). Conclusions ApoE deficiency exacerbates astrocyte injury, likely through promoting the release of pro- inflammatory mediators from mieroglia.
分 类 号:R744.52[医药卫生—神经病学与精神病学]
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