Pulsed radiofrequency inhibited activation of spinal mitogen-activated protein kinases and ameliorated early neuropathic pain in rats

M. L. Lin, W. T. Lin, R. Y. Huang, T. C. Chen, S. H. Huang, C. H. Chang, Shih-Ying Tsai, H. W. Chiu, G. C. Yeh, C. W. Lin, Yeong-Ray Wen

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Background Pulsed radiofrequency (PRF) has been widely used to treat chronic pain, but the effectiveness and mechanisms in preventing early neuropathic pain have not been well explored. Even fewer knowledge is available in its impact on glia-mediated nociceptive sensitization. This study aims to elucidate the modulation of PRF on nerve injury-induced pain development and activation of spinal mitogen-activated protein kinases (MAPKs). Methods In a rat spinal nerve ligation (SNL) model, a low-volt PRF treatment was applied to the L5 dorsal root ganglion after nerve injury. Nociceptive behaviours were measured by von Frey and heat withdrawal tests at multiple time points. MAPK activations, including p-ERK and p-p38, as well as TNF-α level in the spinal dorsal horn were assessed and the cell types that expressed MAPK activation were identified by double immunofluorescence staining. Results We found that SNL promptly induced neuropathic pain in the affected hind limb for over 1 week as well as increased p-ERK and p-p38 in the spinal dorsal horn. PRF significantly attenuated SNL-induced mechanical allodynia and thermal hyperalgesia for 5-7 days. PRF also inhibited ERK and p38 activations, which were found majorly located within neurons and microglia, respectively. Besides, PRF significantly suppressed expression of TNF-α in the spinal dorsal horn throughout the course. Conclusions Low-volt PRF significantly ameliorated SNL-induced acute pain. Inferentially, PRF may inhibit spinal sensitization by down-regulating spinal MAPK activations and activation-mediated cytokine release. We demonstrated that early PRF treatment in acute nerve injury helps to ameliorate neuropathic pain development.

Original languageEnglish
Pages (from-to)659-670
Number of pages12
JournalEuropean Journal of Pain (United Kingdom)
Volume18
Issue number5
DOIs
Publication statusPublished - 2014

Fingerprint

Spinal Nerves
Neuralgia
Mitogen-Activated Protein Kinases
Pulsed Radiofrequency Treatment
Ligation
Hyperalgesia
Wounds and Injuries
Acute Pain
Spinal Ganglia
Microglia
Neuroglia
Chronic Pain
Fluorescent Antibody Technique
Extremities
Hot Temperature
Staining and Labeling
Cytokines
Neurons
Pain
Spinal Cord Dorsal Horn

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine
  • Medicine(all)

Cite this

Pulsed radiofrequency inhibited activation of spinal mitogen-activated protein kinases and ameliorated early neuropathic pain in rats. / Lin, M. L.; Lin, W. T.; Huang, R. Y.; Chen, T. C.; Huang, S. H.; Chang, C. H.; Tsai, Shih-Ying; Chiu, H. W.; Yeh, G. C.; Lin, C. W.; Wen, Yeong-Ray.

In: European Journal of Pain (United Kingdom), Vol. 18, No. 5, 2014, p. 659-670.

Research output: Contribution to journalArticle

Lin, ML, Lin, WT, Huang, RY, Chen, TC, Huang, SH, Chang, CH, Tsai, S-Y, Chiu, HW, Yeh, GC, Lin, CW & Wen, Y-R 2014, 'Pulsed radiofrequency inhibited activation of spinal mitogen-activated protein kinases and ameliorated early neuropathic pain in rats', European Journal of Pain (United Kingdom), vol. 18, no. 5, pp. 659-670. https://doi.org/10.1002/j.1532-2149.2013.00419.x
Lin, M. L. ; Lin, W. T. ; Huang, R. Y. ; Chen, T. C. ; Huang, S. H. ; Chang, C. H. ; Tsai, Shih-Ying ; Chiu, H. W. ; Yeh, G. C. ; Lin, C. W. ; Wen, Yeong-Ray. / Pulsed radiofrequency inhibited activation of spinal mitogen-activated protein kinases and ameliorated early neuropathic pain in rats. In: European Journal of Pain (United Kingdom). 2014 ; Vol. 18, No. 5. pp. 659-670.
@article{3366b929fbbc4ccba3cdaa807a7b054e,
title = "Pulsed radiofrequency inhibited activation of spinal mitogen-activated protein kinases and ameliorated early neuropathic pain in rats",
abstract = "Background Pulsed radiofrequency (PRF) has been widely used to treat chronic pain, but the effectiveness and mechanisms in preventing early neuropathic pain have not been well explored. Even fewer knowledge is available in its impact on glia-mediated nociceptive sensitization. This study aims to elucidate the modulation of PRF on nerve injury-induced pain development and activation of spinal mitogen-activated protein kinases (MAPKs). Methods In a rat spinal nerve ligation (SNL) model, a low-volt PRF treatment was applied to the L5 dorsal root ganglion after nerve injury. Nociceptive behaviours were measured by von Frey and heat withdrawal tests at multiple time points. MAPK activations, including p-ERK and p-p38, as well as TNF-α level in the spinal dorsal horn were assessed and the cell types that expressed MAPK activation were identified by double immunofluorescence staining. Results We found that SNL promptly induced neuropathic pain in the affected hind limb for over 1 week as well as increased p-ERK and p-p38 in the spinal dorsal horn. PRF significantly attenuated SNL-induced mechanical allodynia and thermal hyperalgesia for 5-7 days. PRF also inhibited ERK and p38 activations, which were found majorly located within neurons and microglia, respectively. Besides, PRF significantly suppressed expression of TNF-α in the spinal dorsal horn throughout the course. Conclusions Low-volt PRF significantly ameliorated SNL-induced acute pain. Inferentially, PRF may inhibit spinal sensitization by down-regulating spinal MAPK activations and activation-mediated cytokine release. We demonstrated that early PRF treatment in acute nerve injury helps to ameliorate neuropathic pain development.",
author = "Lin, {M. L.} and Lin, {W. T.} and Huang, {R. Y.} and Chen, {T. C.} and Huang, {S. H.} and Chang, {C. H.} and Shih-Ying Tsai and Chiu, {H. W.} and Yeh, {G. C.} and Lin, {C. W.} and Yeong-Ray Wen",
year = "2014",
doi = "10.1002/j.1532-2149.2013.00419.x",
language = "English",
volume = "18",
pages = "659--670",
journal = "European Journal of Pain",
issn = "1090-3801",
publisher = "W.B. Saunders Ltd",
number = "5",

}

TY - JOUR

T1 - Pulsed radiofrequency inhibited activation of spinal mitogen-activated protein kinases and ameliorated early neuropathic pain in rats

AU - Lin, M. L.

AU - Lin, W. T.

AU - Huang, R. Y.

AU - Chen, T. C.

AU - Huang, S. H.

AU - Chang, C. H.

AU - Tsai, Shih-Ying

AU - Chiu, H. W.

AU - Yeh, G. C.

AU - Lin, C. W.

AU - Wen, Yeong-Ray

PY - 2014

Y1 - 2014

N2 - Background Pulsed radiofrequency (PRF) has been widely used to treat chronic pain, but the effectiveness and mechanisms in preventing early neuropathic pain have not been well explored. Even fewer knowledge is available in its impact on glia-mediated nociceptive sensitization. This study aims to elucidate the modulation of PRF on nerve injury-induced pain development and activation of spinal mitogen-activated protein kinases (MAPKs). Methods In a rat spinal nerve ligation (SNL) model, a low-volt PRF treatment was applied to the L5 dorsal root ganglion after nerve injury. Nociceptive behaviours were measured by von Frey and heat withdrawal tests at multiple time points. MAPK activations, including p-ERK and p-p38, as well as TNF-α level in the spinal dorsal horn were assessed and the cell types that expressed MAPK activation were identified by double immunofluorescence staining. Results We found that SNL promptly induced neuropathic pain in the affected hind limb for over 1 week as well as increased p-ERK and p-p38 in the spinal dorsal horn. PRF significantly attenuated SNL-induced mechanical allodynia and thermal hyperalgesia for 5-7 days. PRF also inhibited ERK and p38 activations, which were found majorly located within neurons and microglia, respectively. Besides, PRF significantly suppressed expression of TNF-α in the spinal dorsal horn throughout the course. Conclusions Low-volt PRF significantly ameliorated SNL-induced acute pain. Inferentially, PRF may inhibit spinal sensitization by down-regulating spinal MAPK activations and activation-mediated cytokine release. We demonstrated that early PRF treatment in acute nerve injury helps to ameliorate neuropathic pain development.

AB - Background Pulsed radiofrequency (PRF) has been widely used to treat chronic pain, but the effectiveness and mechanisms in preventing early neuropathic pain have not been well explored. Even fewer knowledge is available in its impact on glia-mediated nociceptive sensitization. This study aims to elucidate the modulation of PRF on nerve injury-induced pain development and activation of spinal mitogen-activated protein kinases (MAPKs). Methods In a rat spinal nerve ligation (SNL) model, a low-volt PRF treatment was applied to the L5 dorsal root ganglion after nerve injury. Nociceptive behaviours were measured by von Frey and heat withdrawal tests at multiple time points. MAPK activations, including p-ERK and p-p38, as well as TNF-α level in the spinal dorsal horn were assessed and the cell types that expressed MAPK activation were identified by double immunofluorescence staining. Results We found that SNL promptly induced neuropathic pain in the affected hind limb for over 1 week as well as increased p-ERK and p-p38 in the spinal dorsal horn. PRF significantly attenuated SNL-induced mechanical allodynia and thermal hyperalgesia for 5-7 days. PRF also inhibited ERK and p38 activations, which were found majorly located within neurons and microglia, respectively. Besides, PRF significantly suppressed expression of TNF-α in the spinal dorsal horn throughout the course. Conclusions Low-volt PRF significantly ameliorated SNL-induced acute pain. Inferentially, PRF may inhibit spinal sensitization by down-regulating spinal MAPK activations and activation-mediated cytokine release. We demonstrated that early PRF treatment in acute nerve injury helps to ameliorate neuropathic pain development.

UR - http://www.scopus.com/inward/record.url?scp=84898998487&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84898998487&partnerID=8YFLogxK

U2 - 10.1002/j.1532-2149.2013.00419.x

DO - 10.1002/j.1532-2149.2013.00419.x

M3 - Article

C2 - 25493301

AN - SCOPUS:84898998487

VL - 18

SP - 659

EP - 670

JO - European Journal of Pain

JF - European Journal of Pain

SN - 1090-3801

IS - 5

ER -