大鼠脑缺血/再灌注模型中n -酰基乙醇胺通路相关代谢物的变化

Journal of glycomics & lipidomics Pub Date : 2011-01-01
Aruna Kilaru, Pamela Tamura, Puja Garg, Giorgis Isaac, David Baxter, R Scott Duncan, Ruth Welti, Peter Koulen, Kent D Chapman, Barney J Venables
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引用次数: 0

摘要

在哺乳动物中,内源性大麻素信号通路对缺血提供保护性细胞反应。先前的研究表明,长链n -酰基乙醇胺(NAE)在缺血时增加,并提示NAE具有保护作用。本研究采用靶向脂质组学方法研究了控制性脑缺血大鼠模型中NAE代谢物的分子组成和数量的全面变化。测定NAE及其前体n -酰基磷脂酰乙醇胺(NAPE)、主要磷脂和次要磷脂以及游离脂肪酸(FFA)在缺血后的变化。测定缺血前腹腔注射n -棕榈酰乙醇胺(NAE 16:0)对NAE代谢物和磷脂谱的影响。虽然缺血通常会导致n -酰基16:0和18:0 NAE、NAPE和FFA含量升高,但NAE 16:0预处理会减少梗死面积、大鼠神经行为缺陷和缺血组织中FFA含量。NAE 16:0预处理不影响其他NAE代谢物的谱。这些研究证明了靶向脂质组学方法用于测量缺血反应中复杂和伴随的代谢变化的实用性。他们认为,外源性NAE 16:0的神经保护作用和炎症损伤的减少可能是由脑NAE水平变化以外的因素介导的,比如转录反应的调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Changes in N-acylethanolamine Pathway Related Metabolites in a Rat Model of Cerebral Ischemia/Reperfusion.

Changes in N-acylethanolamine Pathway Related Metabolites in a Rat Model of Cerebral Ischemia/Reperfusion.

In mammals, the endocannabinoid signaling pathway provides protective cellular responses to ischemia. Previous work demonstrated increases in long-chain N-acylethanolamines (NAE) in ischemia and suggested a protective role for NAE. Here, a targeted lipidomics approach was used to study comprehensive changes in the molecular composition and quantity of NAE metabolites in a rat model of controlled brain ischemia. Changes of NAE, its precursors, N-acylphosphatidylethanolamines (NAPE), major and minor phospholipids, and free fatty acids (FFA) were quantified in response to ischemia. The effect of intraperitoneal injection of N-palmitoylethanolamine (NAE 16:0) prior to ischemia on NAE metabolite and phospholipid profiles was measured. While ischemia, in general, resulted in elevated levels of N-acyl 16:0 and18:0 NAE, NAPE, and FFA species, pretreatment with NAE 16:0 reduced infarct volume, neurological behavioral deficits in rats, and FFA content in ischemic tissues. Pretreatment with NAE 16:0 did not affect the profiles of other NAE metabolites. These studies demonstrate the utility of a targeted lipidomics approach to measure complex and concomitant metabolic changes in response to ischemia. They suggest that the neuroprotective effects of exogenous NAE 16:0 and the reduction in inflammatory damage may be mediated by factors other than gross changes in brain NAE levels, such as modulation of transcriptional responses.

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