文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期，新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2025

膜蛋白Nav1.7在脊髓背根神经节（DRG）的SMIR大鼠模型中，对由p-p65调节的术后持续性疼痛起作用。

Membrane protein Nav1.7 contributes to the persistent post-surgical pain regulated by p-p65 in dorsal root ganglion (DRG) of SMIR rats model.

作者信息

Li Zhisong, Li Yaru, Cao Jing, Han Xuemin, Cai Weihua, Zang Weidong, Xu Jitian, Zhang Wei

机构信息

Department of Anesthesiology, the First Affiliated Hospital, Zhengzhou University, No 1, Jianshe Road, Zhengzhou, 450052, People's Republic of China.

Department of Anatomy, Basic Medical College, Zhengzhou University, No 100, Kexue Road, Zhengzhou, 450001, People's Republic of China.

出版信息

BMC Anesthesiol. 2017 Nov 7;17(1):150. doi: 10.1186/s12871-017-0438-8.

DOI:10.1186/s12871-017-0438-8
PMID:29115943
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5678798/
Abstract

BACKGROUND: Persistent post-surgical pain is a difficult clinical problem. In this study, we intend to explore the mechanism underlying the persistent post-surgical pain in SMIR (skin/muscle incision and retraction) rats. METHODS: First of all, the expression of membrane protein Nav1.7 and p-p65 (Phosphorylation of p65) were detected in ipsilateral L4-6 DRGs of SMIR rats by western-blot and immunostaining. Then with ProTx-II (Nav1.7 blocker) or PDTC (p65 inhibitor) were intrathecally injected while the change of Nav1.7 expression and mechanical withdrawal threshold were detected. Finally chromatin immunoprecipitation assay method was used to detect whether could p-p65 bind in the Nav1.7 gene promoter region directly. RESULTS: The results shows that mechanical hyperalgesia occurs following SMIR model, from 5 day (d) and lasted more than 20d after surgery. Meanwhile, the expression of Nav1.7 was up-regulated at 10d, 15d and 20d after surgery compared with naïve group. The expression of p-p65 was up-regulated at 10d and 15d compared with incision group. The mechanical hyperalgesia induced by SMIR was reversed after blocking Nav1.7 or inhibiting p65. Furthermore, Nav1.7 expression was down-regulated when p-p65 was inhibited and p-p65 could combine with the Nav1.7 gene promoter region directly. CONCLUSION: Membrane protein Nav1.7 could participate in the peripheral sensitization of persistent post-surgical pain, which may be regulated by p-p65.

摘要

背景：术后持续性疼痛是一个棘手的临床问题。在本研究中，我们旨在探究皮肤/肌肉切开并牵拉（SMIR）大鼠术后持续性疼痛的潜在机制。 方法：首先，通过蛋白质免疫印迹法和免疫染色检测SMIR大鼠同侧L4-6背根神经节（DRG）中膜蛋白Nav1.7和p-p65（p65磷酸化）的表达。然后鞘内注射ProTx-II（Nav1.7阻断剂）或PDTC（p65抑制剂），同时检测Nav1.7表达变化和机械缩足阈值。最后采用染色质免疫沉淀测定法检测p-p65是否能直接结合在Nav1.7基因启动子区域。 结果：结果显示，SMIR模型术后第5天出现机械性痛觉过敏，并持续超过20天。同时，与未手术组相比，术后第10天、15天和20天Nav1.7表达上调。与切开组相比，术后第10天和15天p-p65表达上调。阻断Nav1.7或抑制p65后，SMIR诱导的机械性痛觉过敏得到逆转。此外，抑制p-p65时Nav1.7表达下调，且p-p65可直接与Nav1.7基因启动子区域结合。 结论：膜蛋白Nav1.7可能参与术后持续性疼痛的外周敏化，这可能受p-p65调控。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/aaefd9bac040/12871_2017_438_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/4dd9c628b235/12871_2017_438_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/629cd6c2ab7e/12871_2017_438_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/83d477cb77c6/12871_2017_438_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/d9d80ef447ce/12871_2017_438_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/aaefd9bac040/12871_2017_438_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/4dd9c628b235/12871_2017_438_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/629cd6c2ab7e/12871_2017_438_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/83d477cb77c6/12871_2017_438_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/d9d80ef447ce/12871_2017_438_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cc8/5678798/aaefd9bac040/12871_2017_438_Fig5_HTML.jpg

相似文献

[1]
Membrane protein Nav1.7 contributes to the persistent post-surgical pain regulated by p-p65 in dorsal root ganglion (DRG) of SMIR rats model.

BMC Anesthesiol. 2017-11-7

[2]
p38 and interleukin-1 beta pathway via toll-like receptor 4 contributed to the skin and muscle incision and retraction-induced allodynia.

J Surg Res. 2015-8

[3]
The role of P2X7R/ERK signaling in dorsal root ganglia satellite glial cells in the development of chronic postsurgical pain induced by skin/muscle incision and retraction (SMIR).

Brain Behav Immun. 2017-11-17

[4]
Forced treadmill running suppresses postincisional pain and inhibits upregulation of substance P and cytokines in rat dorsal root ganglion.

J Pain. 2014-8

[5]
The different mechanisms of peripheral and central TLR4 on chronic postsurgical pain in rats.

J Anat. 2021-7

[6]
TLR4/NF-κB signaling activation in plantar tissue and dorsal root ganglion involves in the development of postoperative pain.

Mol Pain. 2018-10-1

[7]
Characterization of a model of persistent postoperative pain evoked by skin/muscle incision and retraction (SMIR).

Pain. 2008-3

[8]
DRG Voltage-Gated Sodium Channel 1.7 Is Upregulated in Paclitaxel-Induced Neuropathy in Rats and in Humans with Neuropathic Pain.

J Neurosci. 2017-12-18

[9]
Bilateral downregulation of Nav1.8 in dorsal root ganglia of rats with bone cancer pain induced by inoculation with Walker 256 breast tumor cells.

BMC Cancer. 2010-5-20

[10]
shRNA mediated knockdown of Nav1.7 in rat dorsal root ganglion attenuates pain following burn injury.

BMC Anesthesiol. 2016-8-11

引用本文的文献

[1]
Discordance between preclinical and clinical testing of Na V 1.7-selective inhibitors for pain.

Pain. 2025-3-1

[2]
Genome-Wide Expression Profiling by RNA-Sequencing in Spinal Cord Dorsal Horn of a Rat Chronic Postsurgical Pain Model to Explore Potential Mechanisms Involved in Chronic Pain.

J Pain Res. 2022-4-5

[3]
Nociceptor Overexpression of Na1.7 Contributes to Chronic Muscle Pain Induced by Early-Life Stress.

J Pain. 2021-7

[4]
Age-related molecular changes in the lumbar dorsal root ganglia of mice: Signs of sensitization, and inflammatory response.

JOR Spine. 2020-9-13

[5]
NGF-Induced Nav1.7 Upregulation Contributes to Chronic Post-surgical Pain by Activating SGK1-Dependent Nedd4-2 Phosphorylation.

Mol Neurobiol. 2021-3

[6]
Influence of androgenic blockade with flutamide on pain behaviour and expression of the genes that encode the NaV1.7 and NaV1.8 voltage-dependent sodium channels in a rat model of postoperative pain.

J Transl Med. 2019-8-27

[7]
Voltage-gated sodium channel 1.7 expression decreases in dorsal root ganglia in a spinal nerve ligation neuropathic pain model.

Kaohsiung J Med Sci. 2019-5-14

本文引用的文献

[1]
Ctenopharyngodon idella NF-κB subunit p65 modulates the transcription of IκBα in CIK cells.

Fish Shellfish Immunol. 2016-7

[2]
[NF-κB signaling pathways and the future perspectives of bone disease therapy using selective inhibitors of NF-κB].

Clin Calcium. 2016-2

[3]
Voltage gated sodium channels as drug discovery targets.

Channels (Austin). 2015

[4]
Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channels in Primary Sensory Neurons in Rats with Diabetes.

J Neurogastroenterol Motil. 2016-1-31

[5]
Trafficking regulates the subcellular distribution of voltage-gated sodium channels in primary sensory neurons.

Mol Pain. 2015-9-30

[6]
The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential.

Pharmacol Rev. 2015-10

[7]
p38 and interleukin-1 beta pathway via toll-like receptor 4 contributed to the skin and muscle incision and retraction-induced allodynia.

J Surg Res. 2015-8

[8]
Over-expression of P2X7 receptors in spinal glial cells contributes to the development of chronic postsurgical pain induced by skin/muscle incision and retraction (SMIR) in rats.

Exp Neurol. 2014-9-19

[9]
A review of the literature on multiple factors involved in postoperative pain course and duration.

Postgrad Med. 2014-7

[10]
The role of TNF-alpha/NF-kappa B pathway on the up-regulation of voltage-gated sodium channel Nav1.7 in DRG neurons of rats with diabetic neuropathy.

Neurochem Int. 2014-9

文献AI研究员

20分钟写一篇综述，助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索