Journal
BRAIN RESEARCH
Volume 1134, Issue 1, Pages 199-205Publisher
ELSEVIER
DOI: 10.1016/j.brainres.2006.11.080
Keywords
phospholipase A(2); cytokines; TNF-alpha; interleukin-1; phosphatidylcholine; stroke; focal cerebral ischemia
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Funding
- NINDS NIH HHS [R01 NS042008, NS42008] Funding Source: Medline
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Cerebral ischemia initiates an inflammatory response in the brain that is associated with the induction of a variety of cytokines, including tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha/beta (IL-1 alpha/beta) that contributes to stroke injury. Transient middle cerebral artery occlusion (tMCAO) in spontaneously hypertensive rat (SHR) resulted in significant increases in TNF-alpha and IL-1 beta levels. We have previously demonstrated up-regulation of secretory phospholipase A(2) IIA (sPLA(2) IIA) mRNA and protein expression, increased PLA(2) activity, and loss of phosphatidylcholine after 1-h tMCAO and 24-h reperfusion in SHR. Treatment with TNF-a antibody or IL-1 receptor antagonist significantly attenuated infarction volume, sPLA(2) IIA protein expression, PLA(2) activity and significantly restored phosphatidylcholine levels after tMCAO. This suggests that cytokine induction up-regulates sPLA(2) IIA protein expression, resulting in altered lipid metabolism that contributes to stroke injury. (c) 2006 Elsevier B.V. All rights reserved.
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