Vasculitic peripheral neuropathy induced by ischemia-reperfusion in the rat femoral artery involves activation of proinflammatory signaling pathway in the sciatic nerve

Chih Yang Chung, Yi Wei Chang, Chun Jen Huang, Po Kai Wang, Hung Chieh Wan, Yi Ying Lin, Ming Chang Kao

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Ischemia-reperfusion (IR) in the rat femoral artery has been proposed as an experimental model of vasculitic peripheral neuropathy (VPN) which presents neuropathic pain and peripheral nerve injury patterns observed clinically. This study investigates the involvement of the proinflammatory signaling pathway underlying the peripheral mechanisms of VPN. Male Sprague-Dawley rats were allocated to receive either a sham operation or IR. IR was induced by occluding the right femoral artery for 4 h followed by reperfusion periods from 0 to 72 h. The behavioral parameters were assessed at baseline as well as at days 1, 2 and 3 after reperfusion. The time-course analyses of proinflammatory mediators in the sciatic nerves were also performed on rats of the sham group or IR groups with reperfusion periods of 0, 2, 4, 24 and 72 h, respectively. The behavioral data confirmed that this VPN model induced hindpaw mechano-allodynia and heat hyperalgesia as well as impaired hindpaw grip strength. The molecular data revealed that IR in the femoral artery activated the expression of nuclear factor-κB (NF-κB) in the sciatic nerve indicating a neuroinflammatory response. Moreover, IR in the femoral artery increased the expression of proinflammatory cytokines TNF-α and IL-1β in the sciatic nerve. This study elucidated the novel time-course expression profiles of NF-κB and proinflammatory cytokines in VPN induced by IR which may be involved in the development of neuropathic pain. Since NF-κB is a key element during neuroinflammation, strategies targeting the NF-κB signaling pathway may provide therapeutic potential against VPN induced by IR.

Original languageEnglish
Pages (from-to)77-82
Number of pages6
JournalNeuroscience Letters
Volume656
DOIs
Publication statusPublished - Aug 24 2017
Externally publishedYes

Fingerprint

Peripheral Nervous System Diseases
Sciatic Nerve
Femoral Artery
Reperfusion
Ischemia
Hyperalgesia
Neuralgia
Cytokines
Peripheral Nerve Injuries
Hand Strength
Interleukin-1
Sprague Dawley Rats
Theoretical Models
Hot Temperature

Keywords

  • IL-1β
  • Neuroinflammation
  • Neuropathic pain
  • NF-κβ
  • Peripheral arterial disease
  • TNF-α

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Vasculitic peripheral neuropathy induced by ischemia-reperfusion in the rat femoral artery involves activation of proinflammatory signaling pathway in the sciatic nerve. / Chung, Chih Yang; Chang, Yi Wei; Huang, Chun Jen; Wang, Po Kai; Wan, Hung Chieh; Lin, Yi Ying; Kao, Ming Chang.

In: Neuroscience Letters, Vol. 656, 24.08.2017, p. 77-82.

Research output: Contribution to journalArticle

@article{3dd690c21c6048febe91b7aedd8aef70,
title = "Vasculitic peripheral neuropathy induced by ischemia-reperfusion in the rat femoral artery involves activation of proinflammatory signaling pathway in the sciatic nerve",
abstract = "Ischemia-reperfusion (IR) in the rat femoral artery has been proposed as an experimental model of vasculitic peripheral neuropathy (VPN) which presents neuropathic pain and peripheral nerve injury patterns observed clinically. This study investigates the involvement of the proinflammatory signaling pathway underlying the peripheral mechanisms of VPN. Male Sprague-Dawley rats were allocated to receive either a sham operation or IR. IR was induced by occluding the right femoral artery for 4 h followed by reperfusion periods from 0 to 72 h. The behavioral parameters were assessed at baseline as well as at days 1, 2 and 3 after reperfusion. The time-course analyses of proinflammatory mediators in the sciatic nerves were also performed on rats of the sham group or IR groups with reperfusion periods of 0, 2, 4, 24 and 72 h, respectively. The behavioral data confirmed that this VPN model induced hindpaw mechano-allodynia and heat hyperalgesia as well as impaired hindpaw grip strength. The molecular data revealed that IR in the femoral artery activated the expression of nuclear factor-κB (NF-κB) in the sciatic nerve indicating a neuroinflammatory response. Moreover, IR in the femoral artery increased the expression of proinflammatory cytokines TNF-α and IL-1β in the sciatic nerve. This study elucidated the novel time-course expression profiles of NF-κB and proinflammatory cytokines in VPN induced by IR which may be involved in the development of neuropathic pain. Since NF-κB is a key element during neuroinflammation, strategies targeting the NF-κB signaling pathway may provide therapeutic potential against VPN induced by IR.",
keywords = "IL-1β, Neuroinflammation, Neuropathic pain, NF-κβ, Peripheral arterial disease, TNF-α",
author = "Chung, {Chih Yang} and Chang, {Yi Wei} and Huang, {Chun Jen} and Wang, {Po Kai} and Wan, {Hung Chieh} and Lin, {Yi Ying} and Kao, {Ming Chang}",
year = "2017",
month = "8",
day = "24",
doi = "10.1016/j.neulet.2017.07.031",
language = "English",
volume = "656",
pages = "77--82",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",

}

TY - JOUR

T1 - Vasculitic peripheral neuropathy induced by ischemia-reperfusion in the rat femoral artery involves activation of proinflammatory signaling pathway in the sciatic nerve

AU - Chung, Chih Yang

AU - Chang, Yi Wei

AU - Huang, Chun Jen

AU - Wang, Po Kai

AU - Wan, Hung Chieh

AU - Lin, Yi Ying

AU - Kao, Ming Chang

PY - 2017/8/24

Y1 - 2017/8/24

N2 - Ischemia-reperfusion (IR) in the rat femoral artery has been proposed as an experimental model of vasculitic peripheral neuropathy (VPN) which presents neuropathic pain and peripheral nerve injury patterns observed clinically. This study investigates the involvement of the proinflammatory signaling pathway underlying the peripheral mechanisms of VPN. Male Sprague-Dawley rats were allocated to receive either a sham operation or IR. IR was induced by occluding the right femoral artery for 4 h followed by reperfusion periods from 0 to 72 h. The behavioral parameters were assessed at baseline as well as at days 1, 2 and 3 after reperfusion. The time-course analyses of proinflammatory mediators in the sciatic nerves were also performed on rats of the sham group or IR groups with reperfusion periods of 0, 2, 4, 24 and 72 h, respectively. The behavioral data confirmed that this VPN model induced hindpaw mechano-allodynia and heat hyperalgesia as well as impaired hindpaw grip strength. The molecular data revealed that IR in the femoral artery activated the expression of nuclear factor-κB (NF-κB) in the sciatic nerve indicating a neuroinflammatory response. Moreover, IR in the femoral artery increased the expression of proinflammatory cytokines TNF-α and IL-1β in the sciatic nerve. This study elucidated the novel time-course expression profiles of NF-κB and proinflammatory cytokines in VPN induced by IR which may be involved in the development of neuropathic pain. Since NF-κB is a key element during neuroinflammation, strategies targeting the NF-κB signaling pathway may provide therapeutic potential against VPN induced by IR.

AB - Ischemia-reperfusion (IR) in the rat femoral artery has been proposed as an experimental model of vasculitic peripheral neuropathy (VPN) which presents neuropathic pain and peripheral nerve injury patterns observed clinically. This study investigates the involvement of the proinflammatory signaling pathway underlying the peripheral mechanisms of VPN. Male Sprague-Dawley rats were allocated to receive either a sham operation or IR. IR was induced by occluding the right femoral artery for 4 h followed by reperfusion periods from 0 to 72 h. The behavioral parameters were assessed at baseline as well as at days 1, 2 and 3 after reperfusion. The time-course analyses of proinflammatory mediators in the sciatic nerves were also performed on rats of the sham group or IR groups with reperfusion periods of 0, 2, 4, 24 and 72 h, respectively. The behavioral data confirmed that this VPN model induced hindpaw mechano-allodynia and heat hyperalgesia as well as impaired hindpaw grip strength. The molecular data revealed that IR in the femoral artery activated the expression of nuclear factor-κB (NF-κB) in the sciatic nerve indicating a neuroinflammatory response. Moreover, IR in the femoral artery increased the expression of proinflammatory cytokines TNF-α and IL-1β in the sciatic nerve. This study elucidated the novel time-course expression profiles of NF-κB and proinflammatory cytokines in VPN induced by IR which may be involved in the development of neuropathic pain. Since NF-κB is a key element during neuroinflammation, strategies targeting the NF-κB signaling pathway may provide therapeutic potential against VPN induced by IR.

KW - IL-1β

KW - Neuroinflammation

KW - Neuropathic pain

KW - NF-κβ

KW - Peripheral arterial disease

KW - TNF-α

UR - http://www.scopus.com/inward/record.url?scp=85025143136&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85025143136&partnerID=8YFLogxK

U2 - 10.1016/j.neulet.2017.07.031

DO - 10.1016/j.neulet.2017.07.031

M3 - Article

VL - 656

SP - 77

EP - 82

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

ER -