Fig. 5.

ω-3 PUFA supplementation inhibits the HMGB1/ NF-κB pathway in lesioned cortices 3 days after TBI. a Western blot analysis demonstrated that expression levels of HMGB1 in the cytosol, nuclei and in total protein of neurons and microglias from lesioned cortices increased after TBI. ω-3 PUFA supplementation significantly decreased HMGB1 expression in cytosolic and total cellular protein levels (p < 0.05), but not nuclearprotein (p > 0.05). b A significant reduction in NF-κB p65 DNA binding activity was observed in the TBI + ω-3 group compared with the TBI group (p < 0.05). c ω-3 PUFA supplementation significantly inhibited the translocation of NF-κB p65 from the cytosol to the nucleus and reduced NF-κB p65 expression (p < 0.05). ω-3 PUFA supplementation inhibited NF-κB p65 translocation to the nucleus (p < 0.05). d Representative photomicrographs of NF-κB p65 staining in the experimental groups. Values are expressed as mean ± standard deviation (n = 6 per group). N.S., p > 0.05, *p < 0.05, **p < 0.01. Scale bars = 50 μm