Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission

Marie Hennebelle, Zhichao Zhang, Adam H. Metherel, Alex P. Kitson, Yurika Otoki, Christine E. Richardson, Jun Yang, Kin Sing Stephen Lee, Bruce D. Hammock, Liang Zhang, Richard P. Bazinet, Ameer Y. Taha

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14 Scopus citations

Abstract

Linoleic acid (LA; 18:2 n-6), the most abundant polyunsaturated fatty acid in the US diet, is a precursor to oxidized metabolites that have unknown roles in the brain. Here, we show that oxidized LA-derived metabolites accumulate in several rat brain regions during CO2-induced ischemia and that LA-derived 13-hydroxyoctadecadienoic acid, but not LA, increase somatic paired-pulse facilitation in rat hippocampus by 80%, suggesting bioactivity. This study provides new evidence that LA participates in the response to ischemia-induced brain injury through oxidized metabolites that regulate neurotransmission. Targeting this pathway may be therapeutically relevant for ischemia-related conditions such as stroke.

Original languageEnglish (US)
Article number4342
JournalScientific Reports
Volume7
Issue number1
DOIs
StatePublished - Dec 1 2017

ASJC Scopus subject areas

  • General

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    Hennebelle, M., Zhang, Z., Metherel, A. H., Kitson, A. P., Otoki, Y., Richardson, C. E., Yang, J., Lee, K. S. S., Hammock, B. D., Zhang, L., Bazinet, R. P., & Taha, A. Y. (2017). Linoleic acid participates in the response to ischemic brain injury through oxidized metabolites that regulate neurotransmission. Scientific Reports, 7(1), [4342]. https://doi.org/10.1038/s41598-017-02914-7