Fig. 2: Effects of deficiency of α7-nAChRs on mechanical allodynia and cartilage degradation in OA mice.

After receiving intraperitoneal (i.p) injections of 1 mg/kg nicotine or saline once daily for 7 days, both wild-type (WT) mice and α7-nAChRs knockout (KO) mice were injected with 0.3 mg/10 μL MIA in the right knee joint and were injected with nicotine or saline once daily for 3 weeks (A). Mechanical allodynia was measured as a reduced threshold to von Frey hairs (B). The results are represented as mean ± SEM in 10 mice per group. **P < 0.01 versus corresponding control group; ^##P < 0.01 versus corresponding MIA group; ^&P < 0.05 versus WT MIA⁺Nic group, using a two-way repeated-measures ANOVA followed by Tukey’s test. The deficiency of α7-nAChRs did not affect an MIA-induced reduction in withdrawal threshold but diminished the effect of nicotine on MIA-induced mechanical allodynia (C). The results are represented as mean ± SEM in 10 mice per group. **P < 0.01 versus corresponding control group; ^##P < 0.01 versus corresponding MIA group; ^&P < 0.05 versus WT MIA + Nic group, using a two-way ANOVA followed by Tukey’s test. There were representative sections of toluidine blue staining (D) and hematoxylin-eosin staining (E) from WT mice and KO mice. Scale bar = 100 μm. The red arrow indicates that α7-nAChR deficiency in KO mice showed no difference in toluidine blue staining and hematoxylin-eosin staining than WT mice after MIA injection. Nicotine could reduce the MIA-induced increase of cartilage degeneration score (F), aggrecan loss score (G), and Mankin score (H) in WT mice but not in α7-nAChR KO mice. The results are represented as mean ± SEM in 4 mice per group. **P < 0.01 versus corresponding control group; ^##P < 0.01, ^#P < 0.05 versus corresponding MIA group; ^&P < 0.05 versus WT MIA + Nic group, using a two^-way ANOVA followed by Tukey’s test.