Resolvin D1 and E1 promote resolution of inflammation in microglial cells in vitro
Brain, Behavior, and Immunity. 2016-07-01; 55: 249-259
DOI: 10.1016/j.bbi.2015.12.013
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Rey C(1), Nadjar A(2), Buaud B(3), Vaysse C(3), Aubert A(2), Pallet V(2), Layé S(2), Joffre C(4).
Author information:
(1)INRA, Nutrition et Neurobiologie Intégrée, UMR 1286, 33076 Bordeaux, France;
Univ. Bordeaux, Nutrition et Neurobiologie Intégrée, UMR 1286, 33076 Bordeaux,
France; ITERG, Institut des corps gras, 33600 Pessac, France.
(2)INRA, Nutrition et Neurobiologie Intégrée, UMR 1286, 33076 Bordeaux, France;
Univ. Bordeaux, Nutrition et Neurobiologie Intégrée, UMR 1286, 33076 Bordeaux,
France.
(3)ITERG, Institut des corps gras, 33600 Pessac, France.
(4)INRA, Nutrition et Neurobiologie Intégrée, UMR 1286, 33076 Bordeaux, France;
Univ. Bordeaux, Nutrition et Neurobiologie Intégrée, UMR 1286, 33076 Bordeaux,
France. Electronic address: .
Sustained inflammation in the brain together with microglia activation can lead
to neuronal damage. Hence limiting brain inflammation and activation of microglia
is a real therapeutic strategy for inflammatory disease. Resolvin D1 (RvD1) and
resolvin E1 (RvE1) derived from n-3 long chain polyunsaturated fatty acids are
promising therapeutic compounds since they actively turn off the systemic
inflammatory response. We thus evaluated the anti-inflammatory activities of RvD1
and RvE1 in microglia cells in vitro. BV2 cells were pre-incubated with RvD1 or
RvE1 before lipopolysaccharide (LPS) treatment. RvD1 and RvE1 both decreased
LPS-induced proinflammatory cytokines (TNF-α, IL-6 and IL-1β) gene expression,
suggesting their proresolutive activity in microglia. However, the mechanisms
involved are distinct as RvE1 regulates NFκB signaling pathway and RvD1 regulates
miRNAs expression. Overall, our findings support that pro-resolving lipids are
involved in the resolution of brain inflammation and can be considered as
promising therapeutic agents for brain inflammation.
Copyright © 2015 Elsevier Inc. All rights reserved.