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Article: Corticosterone mediates electroacupuncture-produced anti-edema in a rat model of inflammation

TitleCorticosterone mediates electroacupuncture-produced anti-edema in a rat model of inflammation
Authors
Issue Date2007
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmccomplementalternmed/
Citation
Bmc Complementary And Alternative Medicine, 2007, v. 7 How to Cite?
AbstractBackground: Electroacupuncture (EA) has been reported to produce anti-edema and anti-hyperalgesia effects on inflammatory disease. However, the mechanisms are not clear. The present study investigated the biochemical mechanisms of EA anti-inflammation in a rat model. Methods: Three experiments were conducted on male Sprague-Dawley rats (n = 7-8/per group). Inflammation was induced by injecting complete Freund's adjuvant (CFA) subcutaneously into the plantar surface of one hind paw. Experiment 1 measured plasma corticosterone (CORT) levels to see if EA regulates CORT secretion. Experiment 2 studied the effects of the adrenal gland on the therapeutic actions of EA using adrenalectomy (ADX) rats. Experiment 3 determined whether a prototypical glucocorticoid receptor antagonist, RU486, affects EA anti-edema. EA treatment, 10 Hz at 3 mA and 0.1 ms pulse width, was given twice, for 20 min each, once immediately after CFA administration and again 2 h post-CFA. Plasma CORT levels, paw thickness, indicative of the intensity of inflammation, and paw withdrawal latency (PWL) were measured 2 h and 5 h after the CFA injection. Results: EA significantly increased plasmacorticosterone levels 2 h (5 folds) and 5 h (10 folds) after CFA administration compared to sham EA control, but EA alone in naive rats and CFA alone did not induce significant increases in corticosterone. Adrenalectomy blocked EA-produced anti-edema, but not EA anti-hyperalgesia. RU486 (15 μl, 15 μg/μl), a prototypical glucocorticoid receptor antagonist, also prevented EA anti-edema. Conclusion: The data demonstrate that EA activates the adrenals to increase plasma corticosterone levels and suppress edema and suggest that EA effects differ in healthy subjects and in those with pathologies. © 2007 Li et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/188588
ISSN
2015 Impact Factor: 1.987
2015 SCImago Journal Rankings: 0.783
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Aen_US
dc.contributor.authorZhang, RXen_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorZhang, Hen_US
dc.contributor.authorRen, Ken_US
dc.contributor.authorBerman, BMen_US
dc.contributor.authorTan, Men_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.citationBmc Complementary And Alternative Medicine, 2007, v. 7en_US
dc.identifier.issn1472-6882en_US
dc.identifier.urihttp://hdl.handle.net/10722/188588-
dc.description.abstractBackground: Electroacupuncture (EA) has been reported to produce anti-edema and anti-hyperalgesia effects on inflammatory disease. However, the mechanisms are not clear. The present study investigated the biochemical mechanisms of EA anti-inflammation in a rat model. Methods: Three experiments were conducted on male Sprague-Dawley rats (n = 7-8/per group). Inflammation was induced by injecting complete Freund's adjuvant (CFA) subcutaneously into the plantar surface of one hind paw. Experiment 1 measured plasma corticosterone (CORT) levels to see if EA regulates CORT secretion. Experiment 2 studied the effects of the adrenal gland on the therapeutic actions of EA using adrenalectomy (ADX) rats. Experiment 3 determined whether a prototypical glucocorticoid receptor antagonist, RU486, affects EA anti-edema. EA treatment, 10 Hz at 3 mA and 0.1 ms pulse width, was given twice, for 20 min each, once immediately after CFA administration and again 2 h post-CFA. Plasma CORT levels, paw thickness, indicative of the intensity of inflammation, and paw withdrawal latency (PWL) were measured 2 h and 5 h after the CFA injection. Results: EA significantly increased plasmacorticosterone levels 2 h (5 folds) and 5 h (10 folds) after CFA administration compared to sham EA control, but EA alone in naive rats and CFA alone did not induce significant increases in corticosterone. Adrenalectomy blocked EA-produced anti-edema, but not EA anti-hyperalgesia. RU486 (15 μl, 15 μg/μl), a prototypical glucocorticoid receptor antagonist, also prevented EA anti-edema. Conclusion: The data demonstrate that EA activates the adrenals to increase plasma corticosterone levels and suppress edema and suggest that EA effects differ in healthy subjects and in those with pathologies. © 2007 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.meshAdrenal Glands - Metabolismen_US
dc.subject.meshAdrenalectomyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCorticosterone - 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.meshHormone Antagonists - Pharmacologyen_US
dc.subject.meshHyperalgesia - Drug Therapy - Etiology - Metabolismen_US
dc.subject.meshInflammation - Complications - Metabolism - Therapyen_US
dc.subject.meshMaleen_US
dc.subject.meshMifepristone - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Glucocorticoid - Antagonists & Inhibitorsen_US
dc.subject.meshReference Valuesen_US
dc.titleCorticosterone mediates electroacupuncture-produced anti-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.doi10.1186/1472-6882-7-27en_US
dc.identifier.pmid17697336-
dc.identifier.scopuseid_2-s2.0-34548723303en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34548723303&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume7en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLi, A=16245342100en_US
dc.identifier.scopusauthoridZhang, RX=7404864527en_US
dc.identifier.scopusauthoridWang, Y=7601488320en_US
dc.identifier.scopusauthoridZhang, H=51563012400en_US
dc.identifier.scopusauthoridRen, K=7102272533en_US
dc.identifier.scopusauthoridBerman, BM=35458606800en_US
dc.identifier.scopusauthoridTan, M=55127194900en_US
dc.identifier.scopusauthoridLao, L=7005681883en_US

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