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Authors Liu Y, Wang Z, Han G, Jin L, Zhao P
Received 8 October 2018
Accepted for publication 7 December 2018
Published 23 January 2019 Volume 2019:12 Pages 443—451
DOI https://doi.org/10.2147/JPR.S189353
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 2
Editor who approved publication: Dr E Alfonso Romero-Sandoval
Background: Our
previous study suggested that HBO treatment attenuated neuropathic pain by
inhibiting mTOR to induce autophagy in SNL neuropathic pain model. The aim of
this study was to evaluate the role of AKT/TSC2/mTOR pathway in SNL and
autophagy and determine whether HBO treatment could relieve neuropathic pain
via modulating AKT/TSC2/mTOR pathway.
Materials and methods: Rats were
randomly divided into sham, SNL, SNL + HBO treatment, SNL + vehicle, and SNL +
AKT inhibitor groups. Neuropathic pain was induced following SNL procedure.
Rats in the SNL + HBO group received HBO treatment for 7 consecutive days
beginning on postoperative day 1. The SNL + vehicle group received 10 µL of 3%
dimethyl sulfoxide in saline. SNL + AKT inhibitor group received 10 µL AKT
inhibitor IV intrathecally. Mechanical withdrawal threshold tests were
performed to evaluate mechanical hypersensitivity. AKT, p-AKT, TSC2, mTOR,
p-mTOR, and LC3-II protein expressions were examined by Western blot analysis.
Results: HBO
reversed AKT/TSC2/mTOR upregulation induced by SNL and attenuated neuropathic
pain. Intrathecal injection of AKT inhibitor IV decreased the activity of
AKT/TSC2/mTOR pathway and increased LC3-II expression accompanied by analgesic
effect in SNL rats.
Conclusion: Taken
together, our findings demonstrated AKT/TSC2/mTOR pathway was activated in
SNL-induced neuropathic pain, and HBO treatment attenuated neuropathic pain via
neutralizing AKT/TSC2/mTOR pathway activation.
Keywords: neuropathic
pain, autophagy, mTOR, TSC2, AKT, hyperbaric oxygen