Short communicationsω-3 polyunsaturated fatty acid supplementation ameliorates lipopolysaccharide-induced behavioral deficits and modulates neurotrophic factors in rats: Focus on tPA/PAI-1 system and BDNF-TrkB signaling

- LPS exposure induced depression-like behaviors in rats.
- LPS exposure altered tPA/PAI-1 system and attenuated proBDNF cleavage into mBDNF.
- LPS exposure compromised TrkB activation.
- PUFA treatment restored altered tPA/PAI-1 system and BDNF-TrkB activation.

ω-3 PUFA contains neurotrophic actions, which are associated with its antidepressant properties. In this study, we found that lipopolysaccharide (LPS) exposure induced the rats to a depression-like state and caused disturbances in neurotrophic network, which were partly restored by ω-3 PUFA pretreatment. Given the well-documented role of BDNF in depression, we further assessed the expression of precursor and mature BDNF and proBDNF cleavage-related genes, tissue plasmogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1). We found that ω-3 PUFA supplementation induced tPA and inhibited PAI-1 expression in the LPS-treated rats. While LPS had no effect on proBDNF expression, it markedly suppressed BDNF maturation and TrkB activation. Meanwhile, ω-3 PUFA administration partly enhanced BDNF-TrkB signaling in the inflamed brain. Collectively, our data firstly evaluated the neurotrophic action of ω-3 PUFA in the context of inflammation, highlighting the involvement of tPA/PAI-1 and BDNF-TrkB signaling in the antidepressant effects of ω-3 PUFA.