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. 2019 Nov 21;21(1):320–328. doi: 10.3892/mmr.2019.10839

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Copyright: © Lu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 7. — Effect of CMR on PI3K/AKT signaling in the DRG neurons of diabetic rats. DRG neurons were separated and the lysates were analyzed using western blotting. (A) Expression of PI3K, (B) AKT and p-AKT proteins was detected by western blotting. (C) Relative expression of PI3K (PI3K/GAPDH) was statistically analyzed. (D) Relative expression of p-AKT (p-AKT/AKT) was statistically analyzed. GAPDH was used to confirm equal sample loading. **P<0.01, ***P<0.001 vs. control; ^#P<0.05, ^###P<0.001 vs. model; ^ΔP<0.05 vs. CMR. CMR, Cortex Mori Radicis extract; TRPC1, transient receptor potential canonical channel 1; si-, small interfering RNA; DRG, dorsal root ganglia; P-, phosphorylated.