Dell' Albani P, Condorelli D F, Mudò G, Amico C, Bindoni M, Belluardo N
Institute of Biochemistry, Faculty of Medicine, University of Catania, Italy.
Neurochem Int. 1993 Jun;22(6):567-74. doi: 10.1016/0197-0186(93)90031-y.
In the present paper we analyzed c-fos and zif/268 expression in rat primary astroglial cell cultures after treatment with Platelet-activating Factor (PAF) and its 2-O-methyl-analogue, 1-O-octadecyl-2-O-methoxy-glycero-3-phosphocholine (ET-18-OCH3). Both compounds, at a dose (2 microM) that did not produce toxic effects on astroglial cells, induced a rapid and transient increase of c-fos and zif/268 mRNA level. Pretreatment of astroglial cells with the PAF antagonist BN50730 (5 microM) 10 min prior to the addition of alkyl-phospholipids almost completely prevented the activation of the immediate early genes. On the contrary triazolam, another PAF inhibitor, did not block PAF induced gene expression when added to the medium at 5 microM concentration. ET-18-OCH3 effect on gene expression is blocked by the same antagonist (BN50730) which is effective in inhibiting PAF effect on astrocytes, suggesting that both substances act through the same binding site. Results obtained support the view that astroglial cells are a cellular target for this lipid mediator, and, like macrophages, respond to its methoxy-analogue.
在本论文中，我们分析了用血小板活化因子（PAF）及其2 - O - 甲基类似物1 - O - 十八烷基 - 2 - O - 甲氧基甘油 - 3 - 磷酸胆碱（ET - 18 - OCH3）处理大鼠原代星形胶质细胞培养物后c - fos和zif/268的表达情况。两种化合物在对星形胶质细胞不产生毒性作用的剂量（2微摩尔）下，均诱导了c - fos和zif/268 mRNA水平的快速短暂升高。在添加烷基磷脂前10分钟用PAF拮抗剂BN50730（5微摩尔）预处理星形胶质细胞，几乎完全阻止了即刻早期基因的激活。相反，另一种PAF抑制剂三唑仑以5微摩尔浓度添加到培养基中时，并未阻断PAF诱导的基因表达。ET - 18 - OCH3对基因表达的作用被与抑制PAF对星形胶质细胞作用有效的相同拮抗剂（BN50730）所阻断，这表明两种物质通过相同的结合位点起作用。所获得的结果支持这样一种观点，即星形胶质细胞是这种脂质介质的细胞靶点，并且与巨噬细胞一样，对其甲氧基类似物有反应。
