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. 2017 Sep 8;175(11):1957–1972. doi: 10.1111/bph.13954

Figure 4.

Figure 4

The α9 subtype‐selective peptide RGIA4 and the α7 subtype‐selective peptide ArIB [V11L; V16D] (AR) block the nicotine‐induced proliferation and intracellular signalling of A549 cells. (A–B) The effect of treatment with 100 nM nicotine for 48 h, in the presence or absence of 1 μM RGIA4 (A) (n = 8) and AR (B) (n = 8), on the number of A549 cells. The results are the average of eight experiments performed in triplicate and are expressed as the number of proliferating cells in each well. The statistical analysis was made using one‐way ANOVA followed by a post hoc Bonferroni test (*P < 0.05). (C) Western blot analysis of ERK and Akt pathway activation in A549 cells in the presence or absence of 1 μM RGIA4 (n = 8). The method was the same as that described in part B of Figure 3 except for the fact that 1 μM RGIA4 was used. The Western blotting data were statistically analysed using one‐way ANOVA followed by Dunn's test (*P < 0.05,). (D) Western blot analysis of ERK and Akt pathway activation in A549 cells in the presence or absence of 1 μM AR peptide (n = 8). The method was the same as that described in part B of Figure 3 except for the fact that 1 μM peptide AR was used. The Western blotting data were statistically analysed using one‐way ANOVA followed by Dunn's test (*P < 0.05).