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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Alteration of phosphatidylinositol transfer protein during global brain ischemia-reperfusion in gerbils.
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Alteration of phosphatidylinositol transfer protein during global brain ischemia-reperfusion in gerbils.

机译：沙土鼠全脑缺血再灌注过程中磷脂酰肌醇转移蛋白的变化。

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Phosphatidylinositol transfer proteins (PI-TPs) are responsible for the transport of phosphatidylinositol and other phospholipids. Moreover, these proteins are involved in vesicle transport and in the function of cytoskeleton. Our previous data indicated that brain ischemia affected phosphoinositides metabolism and the level of lipid derived second messengers.In this study, the effect of ischemia-reperfusion injury on the level of PI-TPs and of the role of NMDA receptor stimulation on the alteration of these proteins was investigated during reperfusion after 5min of forebrain ischemia in gerbils. Some groups of animals were injected intraperitoneally with MK-801, an antagonist of NMDA receptor 30min before ischemia. The levels of both PI-TP isoforms alpha+beta and separately the alpha-isoform were determined in cytosol and membrane fraction from brain cortex and hippocampus using Western blot analysis.In the cytosolic fractions, the concentration of both isoforms of PI-TP was 2 times higher when compared to the membrane fraction. In brain cortex, PI-TPalpha isoform consist about 32-44% but in hippocampus 72-82% of both isoforms (PI-TPalpha+beta) in cytosolic and membrane fraction respectively. Ischemia-reperfusion had no effect on PI-TPs in brain cortex. However, in hippocampus after 5min ischemia and during whole reperfusion time up till 7 days the level of PI-TPalpha+beta and PI-TPalpha was significantly higher by about 20-55%, respectively when compared to control. MK-801 eliminated ischemia-reperfusion evoked alteration of PI-TPs. To confirm the role of NMDA receptor in PI-TP alteration additional experiments were carried out on PC-12 cells in culture. The results indicated that activation of NMDA receptor enhances significantly the level of PI-TPalpha. The competitive antagonist of NMDA receptor inhibited this effect. These results indicated that activation of NMDA receptor is connected with PI-TPs alteration and plays an important role in modulation of PI-TPs during ischemia-reperfusion injury that may have important physiopathological consequence.
机译：磷脂酰肌醇转移蛋白（PI-TP）负责磷脂酰肌醇和其他磷脂的运输。此外，这些蛋白质参与囊泡运输和细胞骨架的功能。我们以前的数据表明脑缺血会影响磷酸肌醇的代谢和脂质衍生的第二信使的水平。在这项研究中，缺血再灌注损伤对PI-TP水平的影响以及NMDA受体刺激对这些信号的改变的作用。在沙鼠前脑缺血5分钟后的再灌注过程中研究了蛋白质。缺血前30分钟，向某些动物组腹膜内注射NMDA受体拮抗剂MK-801。使用Western blot分析法测定脑皮质和海马的胞质和膜组分中的PI-TP亚型α+β和单独的α-亚型的水平。在胞质组分中，PI-TP的两种亚型的浓度均为2相较于膜部分，高出三倍。在大脑皮层中，PI-TPalpha同工型分别占胞质和膜组分的两种同工型（PI-TPalpha + beta）的约32-44％，但在海马中。缺血再灌注对脑皮质的PI-TP没有影响。但是，在缺血5分钟后和直到7天的整个再灌注时间内，海马中PI-TPalpha + beta和PI-TPalpha的水平分别比对照组高约20-55％。 MK-801消除了缺血再灌注引起的PI-TP改变。为了证实NMDA受体在PI-TP改变中的作用，在培养的PC-12细胞上进行了另外的实验。结果表明，NMDA受体的活化显着增强了PI-TPα的水平。 NMDA受体的竞争性拮抗剂抑制了该作用。这些结果表明，NMDA受体的激活与PI-TP的改变有关，并且在缺血-再灌注损伤期间对PI-TP的调节中起重要作用，这可能具有重要的生理病理学后果。

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