S-Space College of Veterinary Medicine (수의과대학) Dept. of Veterinary Medicine (수의학과) Journal Papers (저널논문_수의학과)
Low-frequency electroacupuncture suppresses zymosan-induced peripheral inflammation via activation of sympathetic post-ganglionic neurons
- Kim, Hyun-Woo; Kang, Suk-Yun; Yoon, Seo Yeon; Roh, Dae-Hyun; Kwon, Young-Bae; Han, Ho-Jae; Lee, Hye-Jung; Beitze, Alvin J.; Lee, Jang-Hern
- Issue Date
- Brain Res. 1148, 69-75
- Electroacupuncture; Anti-inflammatory; Sympathetic pre-ganglionic neuron; Adrenalectomy; Air pouch; Mouse
- Electroacupuncture (EA) is used to treat a variety of inflammatory diseases; however, the neurophysiological mechanisms underlying EA's anti-inflammatory effect remain unclear. Accumulating evidence suggests that the sympathetic nervous system regulates immunologic and inflammatory responses and thus we hypothesized that this system could be involved in EA's anti-inflammatory effect (EA-AI). The goal of the present study was to evaluate whether the sympathetic nervous system plays a critical role in EA-AI using a mouse air pouch inflammation model. We found that bilateral low-frequency (1 Hz) EA applied to the Zusanli acupoint significantly suppressed the number of zymosan-induced leukocytes migrating into the air pouch. Furthermore, double-labeling immunohistochemical experiments showed that EA stimulation increased Fos expression in choline acetyltransferase (ChAT)-positive sympathetic pre-ganglionic neurons in the intermediolateral region of thoracic spinal cord segments. Chemical sympathetic denervation by intraperitoneal injection of 6-hydroxydopamine (which spares sympathetic adrenal medullary innervation) significantly inhibited EA-AI. In contrast, adrenalectomy did not alter EA-AI. Finally, systemic propranolol administration significantly inhibited EA's anti-inflammatory effect, suggesting that β-adrenoceptors are involved. Collectively, these results suggest that EA produces an anti-inflammatory effect in this mouse air pouch model by activating the sympathetic nervous system leading to the release of catecholamines from post-ganglionic nerve terminals, which act on β-adrenoceptors on immune cells to inhibit their migration.
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