Supplementary Figure 3. STING, TBK1 and IRF3 expression 24h
post-TBI and C-176 administration.
Representative images of STING, p-TBK1 and TBK1 protein expression the
ipsilateral cortex and striatum of mouse brains 24h after
controlled-cortical impact modelling of TBI or sham surgery as detected
by western blot (A-B) . Quantification of total STING(C), phospho-TBK1 (D ), and total TBK1 (E)protein expression relative to β-actin loading control. Protein
expression of STING (C) was significantly decreased in the
cortex and striatum of TBI mice treated with vehicle (cortex p=0.0050,
striatum p=0.0335 and C-176-treated mice (cortex p=0.0062, striatum
p=0.0064) when compared to sham mice 24h-post TBI. No significant
difference was observed in the expression of STING between the
vehicle-treated and the C-176 treated TBI mice. P-TBK1 expression was
significantly decreased in the cortex and striatum of both the
vehicle-treated (cortex p=0.0054, striatum p=0.0202) and the C-176
treated mice (cortex p=0.0350, striatum p=0.0480) compared to sham mice.
Gene expression analysis by qPCR revealed an increased expression of
TMEM173 (F) 24h-post TBI in the cortex of both the vehicle
treated mice (p=0.0002) and the C-176 treated mice (p=0.0057) compared
to sham. Vehicle treated mice also displayed an increased expression of
TMEM173 (p=0.0005). No significant change in the expression of IRF3(G) was detected between all treatment groups. All data is
expressed as mean ± SEM. Significance determined using a one-way ANOVA
with Tukey’s multiple comparison test. **p ≤ 0.01, *** p ≤ 0.001. n = 9
for each treatment group.