Fig. 8

Schematic illustration of the possible neuroprotective mechanisms of ω-3 PUFA supplementation after TBI. As illustrated, TBI-induced microglial activation initiates a neuronal-glial neuroinflammatory response by producing a wide array of pro-inflammatory factors or mediators such as TNF, ILs, and IFN. Under inflammatory conditions, activation of the HMGB1/NF-κB pathway is closely related to its acetylation levels, which is regulated by SIRT1. Supplementation with ω-3PUFA attenuates the inflammatory response by modulating microglial polarization through SIRT1-mediated deacetylation of HMGB1/NF-κB pathway, leading to neuroprotective effects following experimental traumatic brain injury