地塞米松对实验性血管源性脑水肿中游离脂肪酸和二酰基甘油积累的影响。

Neurochemical pathology Pub Date : 1985-01-01
L E Politi, E B Rodriguez de Turco, N G Bazan
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引用次数: 0

摘要

测定右半脑低温诱导脑水肿大鼠左、右半脑游离脂肪酸(FFA)、二酰基甘油(DG)和水分含量。研究了地塞米松预处理的效果。病变24小时后,最大水肿出现,并伴有FFA(8.5倍)和DG(2.9倍)的积累。多不饱和脂肪酸(PUFA),主要是二十二碳六烯酸,在两个脂质池中都显著增加。在对侧半球,只有DG水平增加,特别是含有硬脂酸酯和花生四烯酸酯的DG水平增加了近50%。48小时时,FFA下降60%,而DG达到假水平。这些变化发生在水肿消退之前。地塞米松使两脑半球水肿程度和含pufa的DG的积累减少了30%。损伤侧游离脂肪酸和花生四烯酸的积累被完全抑制。这些结果表明,地塞米松:(1)抑制磷脂酶A2,从而减少膜磷脂分解;(2)对参与PUFA-DG积累的酶系统影响有限。因此,在实验诱导的血管源性脑水肿中,含有pufa的DG可能与水肿液的扩散密切相关,而不是FFA。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dexamethasone effect on free fatty acid and diacylglycerol accumulation during experimentally induced vasogenic brain edema.

Free fatty acids (FFA), diacylglycerols (DG), and water content were measured in the right and left cerebral hemispheres of rats with brain edema cryogenically induced to the right cerebral hemisphere. The effect of dexamethasone pretreatment was also studied. Twenty-four hours after lesion, maximal edema was attained concomitant with an accumulation of FFA (8.5-fold) and DG (2.9-fold). Polyunsaturated fatty acids (PUFA), primarily docosahexaenoic acid, increased greatly in both lipid pools. In the contralateral hemisphere, only DG levels increased, especially those containing stearate and arachidonate, which increased by almost 50%. By 48 h, FFA had decreased 60%, whereas DG had attained sham levels. These changes occurred prior to edema resolution. Dexamethasone decreased the degree of edema and the accumulation of PUFA-containing DG by 30% in both hemispheres. There was a complete inhibition of FFA and arachidonic acid accumulation in the lesioned side. These results suggest that dexamethasone: (1) inhibits phospholipases A2 that, in turn, decrease membrane phospholipid breakdown; and (2) has a limited effect on the enzymatic systems involved in PUFA-DG accumulation. Hence, in experimentally induced vasogenic brain edema, PUFA-containing DG, rather than FFA, may be related closely to the spreading of edema fluid.

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