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Fig. 7 | Molecular Brain

Fig. 7

From: Toll-like receptor 4 deficiency ameliorates β2-microglobulin induced age-related cognition decline due to neuroinflammation in mice

Fig. 7

TLR4 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/6

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