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Article: Electroacupuncture attenuates bone cancer pain and inhibits spinal interleukin-1β expression in a rat model

TitleElectroacupuncture attenuates bone cancer pain and inhibits spinal interleukin-1β expression in a rat model
Authors
Issue Date2007
PublisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.org
Citation
Anesthesia And Analgesia, 2007, v. 105 n. 5, p. 1482-1488 How to Cite?
AbstractBACKGROUND: Although pain affects the quality of life of cancer patients, current medical treatments are either ineffective or have side effects. In the present study we investigated the effect of electroacupuncture (EA) on cancer-induced hyperalgesia and expression of interleukin-1β (IL-1β), upregulation of which is related to the maintenance of persistent pain, in a rat model of bone cancer pain. METHODS: Cancer was induced by injecting AT-3.1 prostate cancer cells into the tibia of male Copenhagen rats. The resulting pain was treated with 10 Hz/2 mA/0.4 ms pulse EA for 30 min daily at the equivalent of the human acupoint GB30 (Huantiao) between Days 14 and 18 after cancer cell inoculation. For sham control, EA needles were inserted into GB30 without stimulation. Thermal hyperalgesia, a decrease in paw withdrawal latency to a noxious thermal stimulus, was measured at baseline and 20 min after EA treatment. IL-1β and its mRNA were respectively determined by immunohistochemistry and reverse transcription-polymerase chain reaction analysis. RESULTS: Thermal hyperalgesia developed between Days 12 and 18 after cancer cell inoculation. EA significantly (P < 0.05) attenuated this hyperalgesia, increasing paw withdrawal latency from 7.0 ± 0.3 s to 9.2 ± 0.4 s, and inhibited the upregulation of IL-1β and its mRNA compared to the sham control. Intrathecal injection of IL-1 receptor antagonist (IL-1ra, 0.1 mg/rat) also significantly inhibited cancer-induced thermal hyperalgesia. CONCLUSION: The data suggest that EA alleviates bone cancer pain, at least in part by suppressing IL-1β expression. The results support the clinical use of EA in the treatment of cancer pain. © 2007 by International Anesthesia Research Society.
Persistent Identifierhttp://hdl.handle.net/10722/188589
ISSN
2023 Impact Factor: 4.6
2023 SCImago Journal Rankings: 1.344
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.authorRen, Ken_US
dc.contributor.authorQiao, JTen_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorLao, Len_US
dc.date.accessioned2013-09-03T04:10:28Z-
dc.date.available2013-09-03T04:10:28Z-
dc.date.issued2007en_US
dc.identifier.citationAnesthesia And Analgesia, 2007, v. 105 n. 5, p. 1482-1488en_US
dc.identifier.issn0003-2999en_US
dc.identifier.urihttp://hdl.handle.net/10722/188589-
dc.description.abstractBACKGROUND: Although pain affects the quality of life of cancer patients, current medical treatments are either ineffective or have side effects. In the present study we investigated the effect of electroacupuncture (EA) on cancer-induced hyperalgesia and expression of interleukin-1β (IL-1β), upregulation of which is related to the maintenance of persistent pain, in a rat model of bone cancer pain. METHODS: Cancer was induced by injecting AT-3.1 prostate cancer cells into the tibia of male Copenhagen rats. The resulting pain was treated with 10 Hz/2 mA/0.4 ms pulse EA for 30 min daily at the equivalent of the human acupoint GB30 (Huantiao) between Days 14 and 18 after cancer cell inoculation. For sham control, EA needles were inserted into GB30 without stimulation. Thermal hyperalgesia, a decrease in paw withdrawal latency to a noxious thermal stimulus, was measured at baseline and 20 min after EA treatment. IL-1β and its mRNA were respectively determined by immunohistochemistry and reverse transcription-polymerase chain reaction analysis. RESULTS: Thermal hyperalgesia developed between Days 12 and 18 after cancer cell inoculation. EA significantly (P < 0.05) attenuated this hyperalgesia, increasing paw withdrawal latency from 7.0 ± 0.3 s to 9.2 ± 0.4 s, and inhibited the upregulation of IL-1β and its mRNA compared to the sham control. Intrathecal injection of IL-1 receptor antagonist (IL-1ra, 0.1 mg/rat) also significantly inhibited cancer-induced thermal hyperalgesia. CONCLUSION: The data suggest that EA alleviates bone cancer pain, at least in part by suppressing IL-1β expression. The results support the clinical use of EA in the treatment of cancer pain. © 2007 by International Anesthesia Research Society.en_US
dc.languageengen_US
dc.publisherLippincott, Williams & Wilkins. The Journal's web site is located at http://www.anesthesia-analgesia.orgen_US
dc.relation.ispartofAnesthesia and Analgesiaen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBone Neoplasms - Complications - Metabolism - Therapyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshElectroacupuncture - Methodsen_US
dc.subject.meshGene Expression Regulation - Physiologyen_US
dc.subject.meshInterleukin-1Beta - Antagonists & Inhibitors - Biosynthesis - Genetics - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshPain - Etiology - Metabolism - Prevention & Controlen_US
dc.subject.meshRatsen_US
dc.subject.meshSpinal Cord - Metabolismen_US
dc.titleElectroacupuncture attenuates bone cancer pain and inhibits spinal interleukin-1β 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.doi10.1213/01.ane.0000284705.34629.c5en_US
dc.identifier.pmid17959986-
dc.identifier.scopuseid_2-s2.0-37349120359en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-37349120359&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume105en_US
dc.identifier.issue5en_US
dc.identifier.spage1482en_US
dc.identifier.epage1488en_US
dc.identifier.isiWOS:000250317500050-
dc.publisher.placeUnited Statesen_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.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridQiao, JT=7103301572en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US
dc.identifier.issnl0003-2999-

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