实验性脊髓损伤后磷脂的降解,花生四烯酸代谢物的形成和脱髓鞘。

L A Horrocks, P Demediuk, R D Saunders, L Dugan, N R Clendenon, E D Means, D K Anderson
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引用次数: 31

摘要

脊髓损伤研究使用猫压缩模型。脂质代谢的早期变化破坏了质膜的完整性,降低了atp酶的活性。高达18%的乙醇胺缩醛原丢失,游离脂肪酸、花生四烯酸、二酰基甘油、前列腺素、血栓烷和白三烯的含量显著升高。这些变化导致水肿、炎症、少突胶质细胞坏死、脱髓鞘和瘫痪。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The degradation of phospholipids, formation of metabolites of arachidonic acid, and demyelination following experimental spinal cord injury.

Spinal cord injury has been studied using a cat compression model. Very early changes in lipid metabolism were found that compromise the integrity of the plasma membrane and decrease the activities of ATPases. Up to 18% of the ethanolamine plasmalogens are lost, with very marked elevations of the free fatty acids, arachidonic acid, diacylglycerols, prostaglandins, thromboxanes, and leukotrienes. These changes result in edema, inflammation, necrosis of oligodendroglia, demyelination, and paralysis.

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