花生四烯酸的脂质过氧化物对大鼠脑微血管中ATP酶活性的增强作用。

Enhancement of ATPase activity by a lipid peroxide of arachidonic acid in rat brain microvessels.

作者信息

Koide T, Asano T, Matsushita H, Takakura K

出版信息

J Neurochem. 1986 Jan;46(1):235-42. doi: 10.1111/j.1471-4159.1986.tb12952.x.

DOI:10.1111/j.1471-4159.1986.tb12952.x

Abstract

The effects of 15-hydroperoxyarachidonic acid (15-HPAA) on Na+, K+- and Mg+-ATPase activities in the blood-brain barrier (BBB) were examined using rat brain microvessels (MV). 15-HPAA markedly stimulated these ATPase activities in MV at low concentrations whereas the synaptosomal Na+, K+-ATPase activity was inhibited in a dose-dependent manner. Further neurochemical analysis revealed that this stimulatory effect of 15-HPAA in MV was not due to a simple detergent-like action of the compound on the membranes but rather to stimulation of the phospholipase A2 and lipoxygenase activity within MV. In addition, it was shown that free radical reactions were involved in the mechanism. Since such anti-edema drugs as 1,2-bis(nicotinamido)propane were proved to be potent suppressors of the enhanced ATPase activity, further speculations on the role of this effect for ischemic brain edema are offered.

摘要

使用大鼠脑微血管（MV）研究了15 - 氢过氧花生四烯酸（15 - HPAA）对血脑屏障（BBB）中Na +、K + - 和Mg + - ATP酶活性的影响。低浓度时，15 - HPAA显著刺激MV中的这些ATP酶活性，而突触体Na +、K + - ATP酶活性则呈剂量依赖性抑制。进一步的神经化学分析表明，15 - HPAA在MV中的这种刺激作用并非由于该化合物对膜的简单去污剂样作用，而是由于刺激了MV内的磷脂酶A2和脂氧合酶活性。此外，还表明自由基反应参与了该机制。由于诸如1,2 - 双（烟酰胺基）丙烷等抗水肿药物被证明是增强的ATP酶活性的有效抑制剂，因此对这种作用在缺血性脑水肿中的作用进行了进一步推测。