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Article: Electroacupuncture attenuates bone cancer-induced hyperalgesia and inhibits spinal preprodynorphin expression in a rat model

TitleElectroacupuncture attenuates bone cancer-induced hyperalgesia and inhibits spinal preprodynorphin expression in a rat model
Authors
KeywordsAcupuncture
Cancer pain
Dynorphin
Hyperalgesia
Spinal cord
Issue Date2008
PublisherWB Saunders Co Ltd. The Journal's web site is located at http://www.elsevier.com/locate/ejpain
Citation
European Journal Of Pain, 2008, v. 12 n. 7, p. 870-878 How to Cite?
AbstractCancer pain impairs the quality of life of cancer patients, but opioid intervention can cause significant side effects that further decrease quality of life. Although electroacupuncture (EA) has been used to treat cancer pain, its mechanisms are largely unknown. To examine its effects and underlying mechanisms on cancer pain, we injected AT-3.1 prostate cancer cells into the tibia to induce bone cancer in the male Copenhagen rat. The resulting pain was treated with 10 Hz/2 mA/0.4 ms pulse EA for 30 min daily at the point equivalent to the human acupoint GB30 (Huantiao) between days 14 and 18 after the injection. For sham control, EA needles were inserted into GB30 without stimulation. Thermal hyperalgesia, a decrease in paw withdrawal latency (PWL) to a noxious thermal stimulus, and mechanical hyperalgesia, a decrease in paw withdrawal pressure threshold (PWPT), was measured at baseline and 20 min after the EA treatment. Preprodynorphin mRNA and dynorphin were determined by RT-PCR and immunohistochemistry, respectively. Thermal and mechanical hyperalgesia developed ipsilaterally between days 12 and 18 after cancer cell inoculation. EA significantly (P < 0.05) attenuated this hyperalgesia, as shown by increased PWL and PWPT, and inhibited up-regulation of preprodynorphin mRNA and dynorphin compared to sham control. Intrathecal injection of antiserum against dynorphin A (1-17) also significantly inhibited the cancer-induced hyperalgesia. These results suggest that EA alleviates bone cancer pain at least in part by suppressing dynorphin expression, and they support the clinical use of EA in the treatment of cancer pain. © 2008 European Federation of Chapters of the International Association for the Study of Pain.
Persistent Identifierhttp://hdl.handle.net/10722/188605
ISSN
2023 Impact Factor: 3.5
2023 SCImago Journal Rankings: 1.132
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, RXen_US
dc.contributor.authorLi, Aen_US
dc.contributor.authorLiu, Ben_US
dc.contributor.authorWang, Len_US
dc.contributor.authorXin, Jen_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorQiao, JTen_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorLao, Len_US
dc.date.accessioned2013-09-03T04:10:33Z-
dc.date.available2013-09-03T04:10:33Z-
dc.date.issued2008en_US
dc.identifier.citationEuropean Journal Of Pain, 2008, v. 12 n. 7, p. 870-878en_US
dc.identifier.issn1090-3801en_US
dc.identifier.urihttp://hdl.handle.net/10722/188605-
dc.description.abstractCancer pain impairs the quality of life of cancer patients, but opioid intervention can cause significant side effects that further decrease quality of life. Although electroacupuncture (EA) has been used to treat cancer pain, its mechanisms are largely unknown. To examine its effects and underlying mechanisms on cancer pain, we injected AT-3.1 prostate cancer cells into the tibia to induce bone cancer in the male Copenhagen rat. The resulting pain was treated with 10 Hz/2 mA/0.4 ms pulse EA for 30 min daily at the point equivalent to the human acupoint GB30 (Huantiao) between days 14 and 18 after the injection. For sham control, EA needles were inserted into GB30 without stimulation. Thermal hyperalgesia, a decrease in paw withdrawal latency (PWL) to a noxious thermal stimulus, and mechanical hyperalgesia, a decrease in paw withdrawal pressure threshold (PWPT), was measured at baseline and 20 min after the EA treatment. Preprodynorphin mRNA and dynorphin were determined by RT-PCR and immunohistochemistry, respectively. Thermal and mechanical hyperalgesia developed ipsilaterally between days 12 and 18 after cancer cell inoculation. EA significantly (P < 0.05) attenuated this hyperalgesia, as shown by increased PWL and PWPT, and inhibited up-regulation of preprodynorphin mRNA and dynorphin compared to sham control. Intrathecal injection of antiserum against dynorphin A (1-17) also significantly inhibited the cancer-induced hyperalgesia. These results suggest that EA alleviates bone cancer pain at least in part by suppressing dynorphin expression, and they support the clinical use of EA in the treatment of cancer pain. © 2008 European Federation of Chapters of the International Association for the Study of Pain.en_US
dc.languageengen_US
dc.publisherWB Saunders Co Ltd. The Journal's web site is located at http://www.elsevier.com/locate/ejpainen_US
dc.relation.ispartofEuropean Journal of Painen_US
dc.subjectAcupuncture-
dc.subjectCancer pain-
dc.subjectDynorphin-
dc.subjectHyperalgesia-
dc.subjectSpinal cord-
dc.subject.meshAcupuncture Analgesiaen_US
dc.subject.meshAdenocarcinoma - Physiopathology - Secondaryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBone Neoplasms - Physiopathology - Secondaryen_US
dc.subject.meshCell Line, Tumor - Transplantationen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshDynorphins - Antagonists & Inhibitors - Biosynthesis - Genetics - Immunologyen_US
dc.subject.meshElectroacupunctureen_US
dc.subject.meshHyperalgesia - Etiology - Therapyen_US
dc.subject.meshImmune Seraen_US
dc.subject.meshImmunization, Passiveen_US
dc.subject.meshInjections, Spinalen_US
dc.subject.meshMaleen_US
dc.subject.meshPain Thresholden_US
dc.subject.meshProtein Precursors - Biosynthesis - Geneticsen_US
dc.subject.meshRatsen_US
dc.subject.meshReaction Timeen_US
dc.subject.meshSpinal Cord - Metabolismen_US
dc.subject.meshTibiaen_US
dc.titleElectroacupuncture attenuates bone cancer-induced hyperalgesia and inhibits spinal preprodynorphin expression in a rat modelen_US
dc.typeArticleen_US
dc.identifier.emailLao, L: lxlao1@hku.hken_US
dc.identifier.authorityLao, L=rp01784en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.ejpain.2007.12.006en_US
dc.identifier.pmid18221900en_US
dc.identifier.scopuseid_2-s2.0-48349140186en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-48349140186&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume12en_US
dc.identifier.issue7en_US
dc.identifier.spage870en_US
dc.identifier.epage878en_US
dc.identifier.isiWOS:000259375900007-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridZhang, RX=7404864527en_US
dc.identifier.scopusauthoridLi, A=16245342100en_US
dc.identifier.scopusauthoridLiu, B=55720712900en_US
dc.identifier.scopusauthoridWang, L=9036448600en_US
dc.identifier.scopusauthoridXin, J=23104505000en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridQiao, JT=7103301572en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US
dc.identifier.issnl1090-3801-

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