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Endogenous n-3 PUFAs attenuated olfactory bulbectomy-induced behavioral and metabolomic abnormalities in Fat-1 mice

Authors :
Li Tian
Ling Yan
Peng Li
Eero Vasar
Zhiyou Yang
Min-Qing Gu
Cai Song
Juan Xia
Source :
Brain, Behavior, and Immunity. 96:143-153
Publication Year :
2021
Publisher :
Elsevier BV, 2021.

Abstract

Depression is associated with abnormal lipid metabolism, and omega (n)-3 polyunsaturated fatty acids (PUFAs) can effectively treat depression. However, mechanism of lipid metabolism involved in the depressive attenuation remains poorly understood. Olfactory bulbectomy (OB)-induced changes in animal behavior and physiological functions are similar to those observed in depressed patients. Therefore, the present study used wild type (WT) and Fat-1 mice with or without OB to explore whether endogenous n-3 PUFA treatment of depression was through rectifying lipid metabolism, and to discover the possible lipid metabolic pathways. In WT mice, OB enhanced locomotor activity associated with up-regulation of lipid metabolites in the serum, such as phosphatidylcholines, L-a-glutamyl-L-Lysine and coproporphyrinogen III (Cop), which were involved in anti-inflammatory lipid metabolic pathways. OB also increased microglia activation marker CD11b and pro-inflammatory cytokines in the hippocampus. In one of the lipid pathways, increased Cop was significantly correlated with the hyper-activity of the OB mice. These OB-induced changes were markedly attenuated by endogenous n-3 PUFAs in Fat-1 mice. Additionally, increased expressions of anti-inflammatory lipid genes, such as fatty acid desaturase (Fads) and phospholipase A2 group VI (Pla2g6), were found in the hippocampus of Fat-1 mice compared with WT mice. Furthermore, Cop administration increased the production of pro-inflammatory cytokines and nitric oxide in a microglial cell line BV2. In conclusion, endogenous n-3 PUFAs in Fat-1 mice attenuated abnormal behavior in the depression model through restoration of lipid metabolism and suppression of inflammatory response.

Details

ISSN :
08891591
Volume :
96
Database :
OpenAIRE
Journal :
Brain, Behavior, and Immunity
Accession number :
edsair.doi.dedup.....e81115cc311d02daaaf06b7e1af12413
Full Text :
https://doi.org/10.1016/j.bbi.2021.05.024