Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture

Acupuncture or electroacupuncture (EA) has been demonstrated to have a powerful antihypernociceptive effect on inflammatory pain. The attenuation of G protein-coupled receptor kinase 2 (GRK2) in spinal cord and peripheral nociceptor has been widely acknowledged to promote the transition from acute t...

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Main Authors: Huan Liu, Shen-Bin Liu, Qian Li, Huijing Wang, Yan-Qing Wang, Qi-Liang Mao-Ying
Format: Article
Language:English
Published: Hindawi Limited 2015-01-01
Series:Evidence-Based Complementary and Alternative Medicine
Online Access:http://dx.doi.org/10.1155/2015/848603
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spelling doaj-a04ea501f7a3467f81cc1dee83d7f5112020-11-25T00:06:41ZengHindawi LimitedEvidence-Based Complementary and Alternative Medicine1741-427X1741-42882015-01-01201510.1155/2015/848603848603Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of ElectroacupunctureHuan Liu0Shen-Bin Liu1Qian Li2Huijing Wang3Yan-Qing Wang4Qi-Liang Mao-Ying5Department of Integrative Medicine and Neurobiology, State Key Laboratory of Medical Neurobiology, Institute of Acupuncture Research and Institutes of Brain Science, Collaborative Innovation Center for Brain Science, School of Basic Medical Science, Fudan University, Shanghai 200032, ChinaDepartment of Integrative Medicine and Neurobiology, State Key Laboratory of Medical Neurobiology, Institute of Acupuncture Research and Institutes of Brain Science, Collaborative Innovation Center for Brain Science, School of Basic Medical Science, Fudan University, Shanghai 200032, ChinaDepartment of Integrative Medicine and Neurobiology, State Key Laboratory of Medical Neurobiology, Institute of Acupuncture Research and Institutes of Brain Science, Collaborative Innovation Center for Brain Science, School of Basic Medical Science, Fudan University, Shanghai 200032, ChinaDepartment of Pharmacology, School of Basic Medical Science, Fudan University, Shanghai 200032, ChinaDepartment of Integrative Medicine and Neurobiology, State Key Laboratory of Medical Neurobiology, Institute of Acupuncture Research and Institutes of Brain Science, Collaborative Innovation Center for Brain Science, School of Basic Medical Science, Fudan University, Shanghai 200032, ChinaDepartment of Integrative Medicine and Neurobiology, State Key Laboratory of Medical Neurobiology, Institute of Acupuncture Research and Institutes of Brain Science, Collaborative Innovation Center for Brain Science, School of Basic Medical Science, Fudan University, Shanghai 200032, ChinaAcupuncture or electroacupuncture (EA) has been demonstrated to have a powerful antihypernociceptive effect on inflammatory pain. The attenuation of G protein-coupled receptor kinase 2 (GRK2) in spinal cord and peripheral nociceptor has been widely acknowledged to promote the transition from acute to chronic pain and to facilitate the nociceptive progress. This study was designed to investigate the possible role of spinal GRK2 in EA antiallodynic in a rat model with complete Freund’s adjuvant (CFA) induced inflammatory pain. EA was applied to ST36 (“Zusanli”) and BL60 (“Kunlun”) one day after CFA injection. Single EA treatment at day 1 after CFA injection remarkably alleviated CFA induced mechanical allodynia two hours after EA. Repeated EA displayed significant antiallodynic effect from 2nd EA treatment and a persistent effect was observed during the rest of treatments. However, downregulation of spinal GRK2 by intrathecal exposure of GRK2 antisense 30 mins after EA treatment completely eliminated both the transient and persistent antiallodynic effect by EA treatment. These pieces of data demonstrated that the spinal GRK2 played an important role in EA antiallodynia on inflammatory pain.http://dx.doi.org/10.1155/2015/848603
collection DOAJ
language English
format Article
sources DOAJ
author Huan Liu
Shen-Bin Liu
Qian Li
Huijing Wang
Yan-Qing Wang
Qi-Liang Mao-Ying
spellingShingle Huan Liu
Shen-Bin Liu
Qian Li
Huijing Wang
Yan-Qing Wang
Qi-Liang Mao-Ying
Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture
Evidence-Based Complementary and Alternative Medicine
author_facet Huan Liu
Shen-Bin Liu
Qian Li
Huijing Wang
Yan-Qing Wang
Qi-Liang Mao-Ying
author_sort Huan Liu
title Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture
title_short Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture
title_full Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture
title_fullStr Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture
title_full_unstemmed Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture
title_sort downregulation of spinal g protein-coupled kinase 2 abolished the antiallodynic effect of electroacupuncture
publisher Hindawi Limited
series Evidence-Based Complementary and Alternative Medicine
issn 1741-427X
1741-4288
publishDate 2015-01-01
description Acupuncture or electroacupuncture (EA) has been demonstrated to have a powerful antihypernociceptive effect on inflammatory pain. The attenuation of G protein-coupled receptor kinase 2 (GRK2) in spinal cord and peripheral nociceptor has been widely acknowledged to promote the transition from acute to chronic pain and to facilitate the nociceptive progress. This study was designed to investigate the possible role of spinal GRK2 in EA antiallodynic in a rat model with complete Freund’s adjuvant (CFA) induced inflammatory pain. EA was applied to ST36 (“Zusanli”) and BL60 (“Kunlun”) one day after CFA injection. Single EA treatment at day 1 after CFA injection remarkably alleviated CFA induced mechanical allodynia two hours after EA. Repeated EA displayed significant antiallodynic effect from 2nd EA treatment and a persistent effect was observed during the rest of treatments. However, downregulation of spinal GRK2 by intrathecal exposure of GRK2 antisense 30 mins after EA treatment completely eliminated both the transient and persistent antiallodynic effect by EA treatment. These pieces of data demonstrated that the spinal GRK2 played an important role in EA antiallodynia on inflammatory pain.
url http://dx.doi.org/10.1155/2015/848603
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