An antarctic krill oil-based diet elicits neuroprotective effects by inhibiting oxidative stress and rebalancing the M1/M2 microglia phenotype in a cuprizone model for demyelination

Multiple sclerosis (MS) is a chronic inflammatory disease that affects the central nervous system, and results in the degradation of the myelin sheath. The study investigates the neuroprotective effects of krill oil (KO) on the cuprizone (CPZ)-induced demyelination of the MS mouse model. The results suggested that KO treatment can improve the motor abnormalities and cognitive deficit of MS mice, as demonstrated by the open field, rotarod and Morris water maze tests. Meanwhile, the CPZ-induced demyelination of mice was alleviated after KO treatment and KO can attenuate the CPZ-induced oxidative stress. Furthermore, KO reduces M1 microglia activation and promotes M2 microglia polarization in the corpus callosum. Moreover, our studies indicated that KO diminished histone deacetylase (HDAC)3, phosphorylated signal transducer and activator of transcription (STAT) 3 and NF-kappa B p65 protein expression levels. In conclusion, KO exerts its neuroprotective actions in mice with CPZ-induced demyelination possibly by modulating the HDAC3/STAT3/NF-kappa B signaling pathways.

Automated summary

Krill oil (KO) demonstrates neuroprotective effects in mice with CPZ-induced demyelination possibly through modulation of the HDAC3/STAT3/NF-kappa B signaling pathways.