Neuroprotective effects of DHA-derived peroxidation product 4(RS)-4-F4t-neuroprostane on microglia.

Autor: Geng X; Richard and Loan Hill Department of Biomedical Engineering, University of Illinois at Chicago, Chicago, IL, 60607, USA., Galano JM; Pôle Chimie Balard Recherche, Institut des Biomolécules Max Mousseron, IBMM, UMR 5247, Université de Montpellier, CNRS, ENSCM, Montpellier, France., Oger C; Pôle Chimie Balard Recherche, Institut des Biomolécules Max Mousseron, IBMM, UMR 5247, Université de Montpellier, CNRS, ENSCM, Montpellier, France., Sun GY; Biochemistry Department, University of Missouri, Columbia, MO, 65211, USA., Durand T; Pôle Chimie Balard Recherche, Institut des Biomolécules Max Mousseron, IBMM, UMR 5247, Université de Montpellier, CNRS, ENSCM, Montpellier, France., Lee JC; Richard and Loan Hill Department of Biomedical Engineering, University of Illinois at Chicago, Chicago, IL, 60607, USA. Electronic address: LeeJam@uic.edu.
Jazyk: angličtina
Zdroj: Free radical biology & medicine [Free Radic Biol Med] 2022 May 20; Vol. 185, pp. 1-5. Date of Electronic Publication: 2022 Apr 18.
DOI: 10.1016/j.freeradbiomed.2022.04.002
Abstrakt: The abundance of docosahexaenoic acid (DHA) in brain membrane phospholipids has stimulated studies to explore its role in neurological functions. Upon released from phospholipids, DHA undergoes enzymatic reactions resulting in synthesis of bioactive docosanoids and prostanoids. However, these phospholipids are also prone to non-enzymatic reactions leading to more complex pattern of metabolites. A non-enzymatic oxidized product of DHA, 4(RS)-4-F 4t -Neuroprostane (44FNP), has been identified in cardiac and brain tissues. In this study, we examined effects of the 44FNP on oxidative and inflammatory responses in microglial cells treated with lipopolysaccharide (LPS). The 44FNP attenuated LPS-induced production of reactive oxygen species (ROS) in both primary and immortalized microglia (BV2). It also attenuated LPS-induced inflammation through suppressing NFκB-p65 and levels of iNOS and TNFα. In addition, 44FNP also suppressed LPS-induced mitochondrial dysfunction and upregulated the Nrf2/HO-1 antioxidative pathway. In sum, these findings with microglial cells demonstrated neuroprotective effects of this 44FNP and shed light into the potential of nutraceutical therapy for neurodegenerative diseases.
(Published by Elsevier Inc.)
Databáze: MEDLINE
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