IMAGING MASS SPECTROMETRY REVEALED THE PRODUCTION OF LYSO-PHOSPHATIDYLCHOLINE IN THE INJURED ISCHEMIC RAT BRAIN
IMAGING MASS SPECTROMETRY REVEALED THE PRODUCTION OF LYSO-PHOSPHATIDYLCHOLINE IN THE INJURED ISCHEMIC RAT BRAIN
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DOI：
10.1016/j.neuroscience.2010.03.056
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发表时间：
2010-06-16
期刊：
影响因子：
3.3
通讯作者：
Namba, H.
中科院分区：
文献类型：
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作者：
Koizumi, S.;Yamamoto, S.;Namba, H.
为了制定有效的神经保护策略来对抗缺血性损伤，确定参与损伤进展的关键分子是很重要的。使用质谱（MS）对组织进行直接分子分析是代谢组学领域非常感兴趣的课题。最值得注意的是，成像质谱（IMS）可以可视化组织表面的分子分布。为了了解缺血性损伤过程中的脂质动力学，我们对局灶性脑缺血大鼠脑组织切片进行了IMS分析。Sprague-Dawley大鼠大脑中动脉闭塞后24 h处死，制作脑切片。IMS分析采用基质辅助激光解吸/电离飞行时间质谱仪（MALDI-TOF MS）在正离子模式下进行。为了确定其分子结构，对检测到的离子进行串联质谱分析。局灶性脑缺血区与正常脑区相比，m/z 798.5和m/z 760.5显示为磷脂酰胆碱、PC（16:0/18:1）的离子信号强度计数降低。相比之下，在局灶性脑缺血区，m/z 496.3的信号明显增加，确定为溶磷脂酰胆碱，LPC（16:0）。在IMS分析中，PC（16:0/18:1）和LPC（16:0）的变化超出了受伤区域的边界。结合先前的报道，PC被磷脂酶A(2) （PLA(2)）水解并产生LPC，我们目前的结果表明，LPC（16:0）是在脑缺血后的损伤过程中产生的，可能是通过PLA(2)的激活，而PC（16:0/18:1）是其前体分子之一。(c) 2010 ibro。Elsevier Ltd.出版。版权所有。
To develop an effective neuroprotective strategy against ischemic injury, it is important to identify the key molecules involved in the progression of injury. Direct molecular analysis of tissue using mass spectrometry (MS) is a subject of much interest in the field of metabolomics. Most notably, imaging mass spectrometry (IMS) allows visualization of molecular distributions on the tissue surface. To understand lipid dynamics during ischemic injury, we performed IMS analysis on rat brain tissue sections with focal cerebral ischemia. Sprague-Dawley rats were sacrificed at 24 h after middle cerebral artery occlusion, and brain sections were prepared. IMS analyses were conducted using matrix-assisted laser desorption/ionization time-of-flight mass spectrometer (MALDI-TOF MS) in positive ion mode. To determine the molecular structures, the detected ions were subjected to tandem MS. The intensity counts of the ion signals of m/z 798.5 and m/z 760.5 that are revealed to be a phosphatidylcholine, PC (16:0/18:1) are reduced in the area of focal cerebral ischemia as compared to the normal cerebral area. In contrast, the signal of m/z 496.3, identified as a lyso-phosphatidylcholine, LPC (16:0), was clearly increased in the area of focal cerebral ischemia. In IMS analyses, changes of PC (16:0/18:1) and LPC (16:0) are observed beyond the border of the injured area. Together with previous reports-that PCs are hydrolyzed by phospholipase A(2) (PLA(2)) and produce LPCs,-our present results suggest that LPC (16:0) is generated during the injury process after cerebral ischemia, presumably via PLA(2) activation, and that PC (16:0/18:1) is one of its precursor molecules. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.