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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



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.


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.


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.


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.