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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 8. — Schematic diagram of proposed mechanism for the neuroregenerative effect of CMR in diabetic rats. CMR treatment increases the expression of TRPC1. As a result, Ca²⁺ influx is decreased. The upregulation of TRPC1 enhanced PI3K activation and AKT phosphorylation, promoting neurite outgrowth of dorsal root ganglia neurons in diabetic rats indicating a potential new biological effect of CMR in enhancing neurite outgrowth and suggesting its potential as an alternative drug for the treatment of diabetic peripheral neuropathy in patients with type II diabetes. NGF, nerve growth factor; CMR, Cortex Mori Radicis extract; TRPC1, transient receptor potential canonical channel 1.