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Original Research Article | OPEN ACCESS

Inhibition of miR-665 alleviates neuropathic pain by targeting SOCS1

Yongqiang Lin1, Mengjia Li2 , Gaofeng Rao1, Wenfu Zhang1, Xuyan Chen3

1Department of Rehabilitation Medicine; 2Department of Medical Laboratory Science, The First People's Hospital of Wenling, The Affiliated Wenling Hospital of Wenzhou Medical University, Taizhou City, Zhejiang Province 317500; 3Department of Physical Medicine & Rehabilitation, The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou City, Zhejiang Province 325000, China.

For correspondence:-  Mengjia Li   Email: QOI5cx@163.com   Tel:+8657689668210

Accepted: 3 August 2020        Published: 31 August 2020

Citation: Lin Y, Li M, Rao G, Zhang W, Chen X. Inhibition of miR-665 alleviates neuropathic pain by targeting SOCS1. Trop J Pharm Res 2020; 19(8):1591-1597 doi: 10.4314/tjpr.v19i8.4

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of miR-665 in neuropathic pain and the possible molecular mechanism involved.
Methods: A neuropathic pain model was established using chronic constriction injury (CCI) methods in Sprague Dawley (SD) rats. Mechanical and thermal hyperalgesia were measured using paw withdrawal threshold (PWT) and paw withdrawal latency (PWL), respectively. The inflammation response was determined by assessing the production of inflammation factors. The target relationship of miR-665 and suppressor of cytokine signaling 1 (SOCS1) was verified by luciferase assay.
Results: In the CCI rat model, PWT and PWL decreased following treatment with miR-665 (p < 0.01). MiR-665 was elevated in the spinal cord and microglia of CCI rats at different time points (p < 0.01). Down-regulation of miR-665 increased PWT and PWL and inhibited the production of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in CCI rats (p < 0.01). Luciferase assay results indicate that SOCS1 was the target of miR-665 (p < 0.01). SOCS1 decreased in CCI rats (p < 0.01) after treatment with miR-665. MiR-665 negatively regulated the expression of SOCS1 (p < 0.01). Down-regulation of SOCS1 reversed the alleviating effect of decreased miR-665 on pain sensitivity and inflammation response (p < 0.01).
Conclusion: Down-regulation of miR-665 alleviates neuropathic pain by targeting SOCS1, and hence making miR-665 a promising therapeutic target for neuropathic pain.

Keywords: MiR-665, SOCS1, Neuropathic pain, CCI, Spinal cord

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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