Abstract | BACKGROUND: 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: 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.
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Authors | Aihui Li, Lixing Lao, Yi Wang, Jiajia Xin, Ke Ren, Brian M Berman, Ming Tan, Ruixin Zhang |
Journal | BMC complementary and alternative medicine
(BMC Complement Altern Med)
Vol. 8
Pg. 20
(May 12 2008)
ISSN: 1472-6882 [Electronic] England |
PMID | 18474100
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Freund's Adjuvant
- Corticotropin-Releasing Hormone
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Topics |
- Analysis of Variance
- Animals
- Corticotropin-Releasing Hormone
(metabolism)
- Disease Models, Animal
- Edema
(etiology, metabolism, prevention & control)
- Electroacupuncture
- Freund's Adjuvant
- Hyperalgesia
(drug therapy, etiology, metabolism)
- Inflammation
(chemically induced, complications, metabolism, therapy)
- Male
- Paraventricular Hypothalamic Nucleus
(metabolism)
- Random Allocation
- Rats
- Rats, Sprague-Dawley
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