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在大鼠慢性压迫性损伤模型中，miR-204-5p通过靶向BRD4减轻神经性疼痛。

MiR-204-5p Alleviates Neuropathic Pain by Targeting BRD4 in a Rat Chronic Constrictive Injury Model.

作者信息

Guo Xiaona, Geng Xia, Chu Yunchao, Gao Jianfei, Jiang Linkai

机构信息

Pain Department, Dongying People's Hospital, Dongying, Shandong, People's Republic of China.

Pain Department, Shengli Oilfield Central Hospital, Dongying, Shandong, People's Republic of China.

出版信息

J Pain Res. 2022 Aug 18;15:2427-2435. doi: 10.2147/JPR.S371616. eCollection 2022.

DOI:10.2147/JPR.S371616
PMID:36003288
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9394659/
Abstract

PURPOSE

The pathogenesis of neuropathic pain is complex, and previous studies have found that microRNAs are important regulators of neuropathic pain and are associated with the progression of neuropathic pain. This study aims to explore the level and role of miR-204-5p in the chronic constrictive injury (CCI) model of rats.

PATIENTS AND METHODS

The CCI rat model was constructed to evaluate paw withdrawal threshold (PWT), paw withdrawal latency (PWL), the expressions of miR-204-5p, and the contents of inflammatory factors in the model. Overexpression of miR-204-5p in rat spinal cord was induced by intrathecal injection of miR-204-5p mimics. PWT and PWL were used to estimate mechanical and thermal pain thresholds. IL-6 and TNF-α were determined by ELISA. Luciferase reporter gene was conducted to verify the targeting relationship between miR-204-5p and BRD4.

RESULTS

miR-204-5p was abnormally down-regulated in the CCI group. The thresholds of mechanical and thermal pain stimulation in the CCI group were lower, and the levels of inflammatory factors were higher than those in the sham group. Overexpression of miR-204-5p alleviated PWT, PWL and inflammatory factors. Besides, the luciferase reporter gene showed that was a target gene of miR-204-5p.

CONCLUSION

These results suggested that miR-204-5p may alleviate neuropathic pain and inflammation through targeted regulation of BRD4 expression.

摘要

目的

神经性疼痛的发病机制复杂，以往研究发现微小RNA是神经性疼痛的重要调节因子，且与神经性疼痛的进展相关。本研究旨在探讨miR-204-5p在大鼠慢性压迫性损伤（CCI）模型中的水平及作用。

患者和方法

构建CCI大鼠模型，评估模型中的 paw withdrawal threshold（PWT）、paw withdrawal latency（PWL）、miR-204-5p的表达以及炎症因子的含量。通过鞘内注射miR-204-5p模拟物诱导大鼠脊髓中miR-204-5p的过表达。PWT和PWL用于评估机械性和热痛阈值。通过ELISA法测定IL-6和TNF-α。进行荧光素酶报告基因实验以验证miR-204-5p与BRD4之间的靶向关系。

结果

CCI组中miR-204-5p异常下调。CCI组的机械性和热痛刺激阈值较低，炎症因子水平高于假手术组。miR-204-5p的过表达减轻了PWT、PWL和炎症因子。此外，荧光素酶报告基因显示[此处原文缺失相关内容]是miR-204-5p的靶基因。

结论

这些结果表明，miR-204-5p可能通过靶向调节BRD4的表达来减轻神经性疼痛和炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/08bab0345574/JPR-15-2427-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/c927e5e86c69/JPR-15-2427-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/3a5bcad57ad4/JPR-15-2427-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/9e4dbe0db5e7/JPR-15-2427-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/23f58dd0413f/JPR-15-2427-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/08bab0345574/JPR-15-2427-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/c927e5e86c69/JPR-15-2427-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/3a5bcad57ad4/JPR-15-2427-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/9e4dbe0db5e7/JPR-15-2427-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/23f58dd0413f/JPR-15-2427-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f230/9394659/08bab0345574/JPR-15-2427-g0005.jpg

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