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长链非编码 RNA LOC100911498 是大鼠神经病理性疼痛的新型调节因子。

Long noncoding RNA LOC100911498 is a novel regulator of neuropathic pain in rats.

机构信息

Department of Anaesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

出版信息

Brain Behav. 2021 Aug;11(8):e01966. doi: 10.1002/brb3.1966. Epub 2021 May 5.

Abstract

INTRODUCTION

Neuropathic pain (NP) is the most debilitating of all clinical pain syndromes and may be a consequence of dysfunction in the somatosensory nervous system. Unfortunately, the pathogenesis of NP is not fully understood yet and it cannot be cured totally. Long noncoding RNA (lncRNA) is a type of RNA molecule greater than 200 nucleotides, and dysregulated expression of lncRNAs play a critical role in the facilitation of NP. Previous study showed the expression level of LOC100911498 in the spinal cords of spared nerve injury (SNI) rats were increased. This research was aimed at exploring what role LOC100911498 plays in the pathophysiological process of NP.

METHODS

The mechanical withdrawal threshold (MWT) of rats was measured by the von Frey test. The expression levels of P2X4 receptor (P2X4R), ionized calcium-binding adaptor molecule 1 (Iba-1), p-p38 and brain-derived neurotrophic factor (BDNF) in spinal cords were detected, respectively.

RESULTS

Our results suggested that the level of LOC100911498 in SNI rats was markedly higher than that in the sham group; the MWT values in rats were treated with LOC100911498siRNA were increased, and the expression levels of P2X4R, Iba-1, p-p38 and BDNF in SNI+ LOC100911498siRNA group were reduced compared with those in the SNI group.

CONCLUSION

Our study indicated the effects lncRNA LOC100911498 siRNA exerted on NP were mediated by P2X4R on microglia in the spinal cords of rats. Further, LOC100911498 may be a novel positive regulator of NP by regulating the expression and function of the P2X4R.

摘要

简介

神经性疼痛(NP)是所有临床疼痛综合征中最使人虚弱的一种,可能是躯体感觉神经系统功能障碍的结果。不幸的是,NP 的发病机制尚未完全了解,目前还不能完全治愈。长链非编码 RNA(lncRNA)是一种大于 200 个核苷酸的 RNA 分子,lncRNA 的表达失调在促进 NP 中起着关键作用。先前的研究表明,在 spared nerve injury(SNI)大鼠的脊髓中,LOC100911498 的表达水平增加。本研究旨在探讨 LOC100911498 在 NP 病理生理过程中的作用。

方法

通过 von Frey 测试测量大鼠的机械退缩阈值(MWT)。分别检测脊髓中 P2X4 受体(P2X4R)、离子钙结合衔接分子 1(Iba-1)、p-p38 和脑源性神经营养因子(BDNF)的表达水平。

结果

我们的结果表明,SNI 大鼠脊髓中 LOC100911498 的水平明显高于假手术组;用 LOC100911498siRNA 处理的大鼠 MWT 值增加,而 SNI+ LOC100911498siRNA 组的 P2X4R、Iba-1、p-p38 和 BDNF 表达水平均低于 SNI 组。

结论

我们的研究表明,lncRNA LOC100911498siRNA 对 NP 的作用是通过大鼠脊髓中的小胶质细胞上的 P2X4R 介导的。此外,LOC100911498 可能通过调节 P2X4R 的表达和功能成为 NP 的新型正调节剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/920b/8413752/3f7a3c54221a/BRB3-11-e01966-g007.jpg

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