Melatonin ameliorates lipopolysaccharide induced brain inflammation through modulation of oxidative status and diminution of cytokine rush in Danio rerio

Lipopolysaccharide (LPS) is known to induce inflammation and immunonomodulation in a piscine model of Danio rerio. Present study aimed to explore the ability of melatonin in attenuating LPS-induced oxidative dam-ages using this model. In LPS-exposed fish, activation of stress marker MDA was observed in brain with corre-sponding augmentation of multiple pro-inflammatory cytokines (IL1 beta, IL6, IL10 and TNF alpha). In addition, it also showed marked increase in the levels of heat shock factor (HSF) and heat shock proteins (HSPs) in association with transcription factors (NF-kB and NRF2) and mitogen-activated protein kinases (MAPKs). The changes in the levels of these mediators are highly correlated with the induction of pro-inflammatory cytokines. In melatonin-treated fishes, significant amelioration of oxidative stress was observed with reduced levels of MDA and pro -inflammatory cytokines. Melatonin also modulated expression of HSPs that facilitated the brain to overcome inflammation-induced stress by directly initiating NFkB/NRF2 translocation. In summary, melatonin effectively functions to reduce stress induced inflammatory signalling through modulation of oxidative stress and protects the brain from the neuropathological insult.

Automated summary

This study investigated the effects of melatonin on attenuating LPS-induced oxidative damages in a zebrafish model. The results showed that melatonin treatment reduced oxidative stress and pro-inflammatory cytokines, protecting the brain from inflammation-induced damage.