Direct profiling of phospholipids and lysophospholipids in rat brain sections after ischemic stroke.
Stroke, a deleterious cerebrovascular event, is caused by a critical reduction in the blood flow to the brain parenchyma that leads to brain injury and loss of brain functions. The inflammatory responses following ischemia often aggravate the neurological damage. Several pro-inflammatory mediators released after stroke are closely related to the metabolism of phospholipids. In this study we directly profiled the changes in phospholipids in the infarcted rat cerebral cortex 24 hours after middle cerebral artery occlusion (MCAO) using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Several phosphatidylcholine (PC) species and sphingomyelin (SM) were significantly decreased after infarction. The cationization pattern of the remaining PCs showed a prominent shift from a mostly potassiated or protonated form to a predominantly sodiated pattern. Stroke also elevated the lysophosphatidylcholines (LPCs) and heme in tissue. The isobaric pairs in PC and LPC classes were resolved by masses through their respective alkali metal adducts in the presence of CsCl. The major fatty acyl LPC species were also structurally confirmed by MALDI-MS/MS. Overall, the results described the changes in PC and LPC species in the infarcted rat cortex. The elevated tissue levels of LPCs and heme signify the ongoing pathological lipid breakdown and the state of parenchymal inflammation. The elevated LPC level in tissue suggests a means of intervention through lysophospholipid metabolism that could potentially benefit the management of stroke and other acute neurological injuries.
Wang
Hay-Yan J
HY
Department of Biological Sciences, National Sun Yat-Sen University, 70 Lian-Hai Rd., Kaohsiung 80424, Taiwan. hyjwang@faculty.nsysu.edu.tw
Liu
Cheng Bin
CB
Wu
Hsuan-Wen
HW
Kuo
Jr Shin
JS
D000818:Animals; D001921:Brain / Q000378:metabolism*; D001923:Brain Chemistry; D002545:Brain Ischemia / Q000150:complications*; D004195:Disease Models, Animal; D006801:Humans; D008246:Lysophospholipids / Q000032:analysis / Q000378:metabolism*; D008297:Male; D010743:Phospholipids / Q000032:analysis / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D019032:Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; D020521:Stroke / Q000209:etiology / Q000378:metabolism*
D008246:Lysophospholipids; D010743:Phospholipids