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Article: Electroacupuncture activates corticotrophin-releasing hormone-containing neurons in the paraventricular nucleus of the hypothalammus to alleviate edema in a rat model of inflammation

TitleElectroacupuncture activates corticotrophin-releasing hormone-containing neurons in the paraventricular nucleus of the hypothalammus to alleviate edema in a rat model of inflammation
Authors
Issue Date2008
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccomplementalternmed/
Citation
Bmc Complementary And Alternative Medicine, 2008, v. 8 How to Cite?
AbstractBackground: Studies show that electroacupuncture (EA) has beneficial effects in patients with inflammatory diseases. This study investigated the mechanisms of EA anti-inflammation, using a rat model of complete Freund's adjuvant (CFA)-induced hind paw inflammation and hyperalgesia. Design: Four experiments were conducted on male Sprague-Dawley rats (n = 6-7/per group). Inflammation was induced by injecting CFA into the plantar surface of one hind paw. Experiment 1 examined whether EA increases plasma adrenocorticotropic hormone (ACTH) levels. Experiments 2 and 3 studied the effects of the ACTH and corticotropin-releasing hormone (CRH) receptor antagonists, ACTH(11-24) and astressin, on the EA anti-edema. Experiment 4 determined whether EA activates CRH neurons in the paraventricular nucleus of the hypothalammus. EA treatment, 10 Hz at 3 mA and 0.1 ms pulse width, was given twice for 20 min each, once immediately post and again 2 hr post-CFA. Plasma ACTH levels, paw thickness, and paw withdrawal latency to a noxious thermal stimulus were measured 2 h and 5 h after the CFA. Results: EA significantly increased ACTH levels 5 h (2 folds) after CFA compared to sham EA control, but EA alone in naive rats and CFA alone did not induce significant increases in ACTH. ACTH(11-24) and astressin blocked EA anti-edema but not EA anti-hyperalgesia. EA induced phosphorylation of NR1, an essential subunit of the N-methyl-D-aspartic acid (NMDA) receptor, in CRH-containing neurons of the paraventricular nucleus. Conclusion: The data demonstrate that EA activates CRH neurons to significantly increase plasma ACTH levels and suppress edema through CRH and ACTH receptors in a rat model of inflammation. © 2008 Li et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/188603
ISSN
2015 Impact Factor: 1.987
2015 SCImago Journal Rankings: 0.783
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Aen_US
dc.contributor.authorLao, Len_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorXin, Jen_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorTan, Men_US
dc.contributor.authorZhang, Ren_US
dc.date.accessioned2013-09-03T04:10:32Z-
dc.date.available2013-09-03T04:10:32Z-
dc.date.issued2008en_US
dc.identifier.citationBmc Complementary And Alternative Medicine, 2008, v. 8en_US
dc.identifier.issn1472-6882en_US
dc.identifier.urihttp://hdl.handle.net/10722/188603-
dc.description.abstractBackground: Studies show that electroacupuncture (EA) has beneficial effects in patients with inflammatory diseases. This study investigated the mechanisms of EA anti-inflammation, using a rat model of complete Freund's adjuvant (CFA)-induced hind paw inflammation and hyperalgesia. Design: Four experiments were conducted on male Sprague-Dawley rats (n = 6-7/per group). Inflammation was induced by injecting CFA into the plantar surface of one hind paw. Experiment 1 examined whether EA increases plasma adrenocorticotropic hormone (ACTH) levels. Experiments 2 and 3 studied the effects of the ACTH and corticotropin-releasing hormone (CRH) receptor antagonists, ACTH(11-24) and astressin, on the EA anti-edema. Experiment 4 determined whether EA activates CRH neurons in the paraventricular nucleus of the hypothalammus. EA treatment, 10 Hz at 3 mA and 0.1 ms pulse width, was given twice for 20 min each, once immediately post and again 2 hr post-CFA. Plasma ACTH levels, paw thickness, and paw withdrawal latency to a noxious thermal stimulus were measured 2 h and 5 h after the CFA. Results: EA significantly increased ACTH levels 5 h (2 folds) after CFA compared to sham EA control, but EA alone in naive rats and CFA alone did not induce significant increases in ACTH. ACTH(11-24) and astressin blocked EA anti-edema but not EA anti-hyperalgesia. EA induced phosphorylation of NR1, an essential subunit of the N-methyl-D-aspartic acid (NMDA) receptor, in CRH-containing neurons of the paraventricular nucleus. Conclusion: The data demonstrate that EA activates CRH neurons to significantly increase plasma ACTH levels and suppress edema through CRH and ACTH receptors in a rat model of inflammation. © 2008 Li et al; licensee BioMed Central Ltd.en_US
dc.languageengen_US
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccomplementalternmed/en_US
dc.relation.ispartofBMC Complementary and Alternative Medicineen_US
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCorticotropin-Releasing Hormone - Metabolismen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshEdema - Etiology - Metabolism - Prevention & Controlen_US
dc.subject.meshElectroacupunctureen_US
dc.subject.meshFreund's Adjuvanten_US
dc.subject.meshHyperalgesia - Drug Therapy - Etiology - Metabolismen_US
dc.subject.meshInflammation - Chemically Induced - Complications - Metabolism - Therapyen_US
dc.subject.meshMaleen_US
dc.subject.meshParaventricular Hypothalamic Nucleus - Metabolismen_US
dc.subject.meshRandom Allocationen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.titleElectroacupuncture activates corticotrophin-releasing hormone-containing neurons in the paraventricular nucleus of the hypothalammus to alleviate edema in a rat model of inflammationen_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.doi10.1186/1472-6882-8-20en_US
dc.identifier.pmid18474100-
dc.identifier.scopuseid_2-s2.0-44649172510en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-44649172510&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume8en_US
dc.identifier.isiWOS:000262744000001-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLi, A=16245342100en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US
dc.identifier.scopusauthoridWang, Y=7601488320en_US
dc.identifier.scopusauthoridXin, J=23104505000en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridTan, M=55127194900en_US
dc.identifier.scopusauthoridZhang, R=7404864527en_US

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