Fig. 7From: Toll-like receptor 4 deficiency ameliorates β2-microglobulin induced age-related cognition decline due to neuroinflammation in miceTLR4 elimination decreased the neuroinflammation, apoptosis, increased the level of synaptic proteins and neurotrophic factors following B2M treatment in cultured primary neurons. B2M treatment increased the expression of IL-1β, TNF-α, cleaved-caspase3, and decreased the level of SYN, PSD-95, NGF BDNF and Bcl-2/Bax ratio, which was attenuated in TLR4-KO neurons. a-e Western blot analysis of IL-1β, TNF-α, SYN and PSD-95 in cultured primary neurons, β-actin was used as an internal control(n = 6/subgroup). f-h Western blot analysis of apoptosis-related proteins cleaved-caspase-3, Bax and Bcl-2 in cultured primary neurons, β-actin was used as an internal control(n = 6/subgroup). i-k Western blot analysis of NGF and BDNF in cultured primary neurons, β-actin was used as an internal control(n = 6/subgroup). The data were analyzed using two-way ANOVAs used Tukey’s multiple comparisons test. Values are presented as the means ± SD. Significant differences are expressed as follows: *p < 0.05 compared B2M group vs. Veh group in WT and TLR4-KO mice, according to the two-way ANOVA; #p < 0.05 compared B2M group in TLR4-KO mice vs. WT mice, according to the two-way ANOVA. WT = wild type C57BL/6Back to article page