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

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 CO(2)-induced ischemia and that LA...

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Detalles Bibliográficos
Autores principales: Hennebelle, Marie, Zhang, Zhichao, Metherel, Adam H., Kitson, Alex P., Otoki, Yurika, Richardson, Christine E., Yang, Jun, Lee, Kin Sing Stephen, Hammock, Bruce D., Zhang, Liang, Bazinet, Richard P., Taha, Ameer Y.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5489485/
https://www.ncbi.nlm.nih.gov/pubmed/28659576
http://dx.doi.org/10.1038/s41598-017-02914-7
Descripción
Sumario: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 CO(2)-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.

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