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作 者:周海红[1] 肖亚[1] 陈倍楚[1] 贾真[1] 赵斌[1]
出 处:《神经疾病与精神卫生》2011年第4期362-364,共3页Journal of Neuroscience and Mental Health
基 金:2009年湛江市科技计划项目(2009C3102023)
摘 要:目的通过观察缺氧环境中原代培养大鼠小胶质细胞生物学功能的变化,进一步探讨活化态小胶质细胞在缺血缺氧性脑病中的作用机制。方法通过建立原代培养的SD大鼠小胶质细胞的缺氧模型,观察细胞形态学及其增殖活力的改变。利用ELSIA检测TNF—α、IL-18含量改变,利用荧光探针DAF—FMDA检测iNOS的相对活性。结果在缺氧旱期,原代培养小胶质细胞增殖在缺氧早期开始,增殖活力于缺氧3h时最高,其后随着缺氧时间的延长而降低。在缺氧早期小胶质细胞培养上清液内TNF-α、1L-1β含量以及iNOS相对活性等多种神经毒性因子的表达水平增加。结论缺氧可诱使小胶质细胞生物学功能改变,呈现应激活化状态,主要表现在细胞生长增殖活力先上调后下降,神经毒性因子表达水平显著增高等方面。Objective To study biological function of primary cultured microglia cells in different stages during anoxia,and further discuss activated microglia cells in hypoxic ischemic encephalopathy in the mechanism of action. Methods The morphology and proliferation of microglia cells primary cultured in hypoxie condition were observed. The intracellular TNF-α,IL-1β and iNOS were assayed with ELSIA or fluorescent probe DAF-- FMDA. Results The microglia cells showed attenuated proliferative capability in the early time and decreased persistently following prolongation of the hypoxic time, but increased TNF- α and IL-1β expression as well as the relative activity of iNOS. Conclusions Anoxia can change microglia cells to stress activated state,including initial promotion and subsequent decline in cell proliferation; a significant increase in the expression of the neurotoxic factors; and a alteration in structure and function of mitochondria.
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