Fig. 3

α7 nAchR activation resulted in inhibition of the NF-κB signaling pathway and astrogliosis. a Pretreatment with GTS21 (15 and 30 μm) resulted in reduction of phosphorylated form of IκBα in LPS (60 ng/ml)-treated astrocytes for 30 min. b Treatment of astrocytes with LPS (60 ng/ml) for 3 h caused robust nuclear translocation of NF-κB and pretreatment with α7 nAchR agonist GTS21 (30 μm) for 1 h caused significant reduction in NF-κB nuclear translocation, *p < 0.05 (one-way ANOVA with adjustment for multiple comparisons using Dunnett’s test for the comparison of LPS alone group and GTS21+LPS group as percentage of LPS alone group). Error bars represent SD (n = 6 wells, 50 fields/well). c Treatment with GTS21 (30 μm) reduced the number of processes in LPS (60 ng/ml for 24 h)-activated astrocytes suggesting reduction in reactive astrogliosis. d Pretreatment of GTS21 with 7.5, 15, and 30 μm for 1 h resulted in a dose-dependent decrease in LPS (60 ng/ml for 72 h)-induced levels of nitrites further confirming anti-inflammatory properties of α7 nAchR activation. *p < 0.05 compared with control, ^# p < 0.05 compared with LPS, 60 ng/ml treatment (both using one-way ANOVA with adjustment for multiple comparisons using Tukey’s test). Error bars represent SD (n = 6)