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. 2020 Jan 6;12(1):543–570. doi: 10.18632/aging.102640

Figure 12.

Figure 12

Activation of α7 nAChR activates the calcium signaling pathway in Aβ oligomer and KN93-treated neurons. Protein levels in each group were determined by western blot analysis and β-actin was used as an internal control. The x-axis indicates the Control, hippocampus cells of the WT rat; Control + KN93, the WT hippocampus cells treated with CaMKII inhibitor (KN93); Control + Aβ, the WT hippocampus cells treated with Aβ; Control + PNU, the WT hippocampus cells treated with PNU; PNU + Aβ, the WT hippocampus cells treated with PNU and Aβ; KN93+PNU+Aβ, the WT hippocampus cells treated with KN93, PNU and Aβ; KN93+PNU, the WT hippocampus cells treated with KN93 and PNU; KN93+Aβ, the control group treated with KN93 and Aβ. The Y-axis indicates the protein expression levels as a percentage of the control. The results demonstrated that the protein expression of CaMKIIα was significantly decreased in KN93 or Aβ oligomer-treated neurons, whereas expression of CaMKIIα was increased in the PNU groups (PNU+Aβ, KN93+PNU+Aβ and KN93+PNU). This result indicated that α7 nAChR activated the CaM-CaMKII-CREB signaling pathway. Data are presented as the mean ± standard deviation. *P<0.05, **P<0.01 vs. control; #P<0.05, ##P<0.01 vs. Control+Aβ, △△P<0.01 vs. Control+KN93.