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Open Access Research article

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

Aihui Li1, Rui-Xin Zhang1, Yi Wang2, Haiqing Zhang1, Ke Ren3, Brian M Berman1, Ming Tan4 and Lixing Lao1*

Author Affiliations

1 Center for Integrative Medicine, School of Medicine, University of Maryland, Baltimore, MD 21201 USA

2 Shanghai University of Traditional Chinese Medicine, Yueyang Affiliated Hospital, Shanghai, China

3 Dept. of Biomedical Sciences, Dental School, University of Maryland, Baltimore, MD 21201 USA

4 Division of Biostatistics, University of Maryland Greenebaum Cancer Center, Baltimore, MD 21201 USA

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BMC Complementary and Alternative Medicine 2007, 7:27  doi:10.1186/1472-6882-7-27

Published: 14 August 2007

Abstract

Background

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 plasma corticosterone 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.