전침자극(電鍼刺戟)의 Collagen 유발 관절염(關節炎) 동물(動物)모델에 대한 진통효과(鎭痛效果) 및 기전(機轉)에 관한 연구(硏究) -Serotonergic Mechanism을 중심으로-

The Analgesic Effect and Its Mechanism of Electroacupuncture in the Type II Collagen-induced Arthritis Rats : Mediation by Serotonergic Receptors

  • 류성룡 (경희대학교 한의과대학 침구학교실) ;
  • 백용현 (경희대학교 한의과대학 침구학교실) ;
  • 박동석 (경희대학교 한의과대학 침구학교실)
  • Ryu, Seong-Ryong (Department of Acupuncture and Moxibustion, College of Oriental Medicine, Kyunghee University) ;
  • Baek, Yong-Hyeon (Department of Acupuncture and Moxibustion, College of Oriental Medicine, Kyunghee University) ;
  • Park, Dong-Suk (Department of Acupuncture and Moxibustion, College of Oriental Medicine, Kyunghee University)
  • 발행 : 2006.06.20

초록

Objectives : To evaluate the analgesic effect of electroacupuncture on Choksamni (ST36) in the collagen-induced arthritis rats and investigate the role played by serotonergic receptor subtypes $(5-HT_{1A},\;5-HT_{1B},\;5-HT_4)$ in the antinociceptive effect of electroacupuncture in the thermal hyperalgesia test. Methods : Immunization of male Sprague-Dawley rats with bovine type II collagen emulsified in incomplete Freund's adjuvant, followed by booster injection 14 days later induced collagen-induced arthritis (CIA). The thermal hyperalgesia was evaluated weekly with tail flick latency (TFL). In the fourth week after first immunization. EA stimulation (2Hz, 0.07mA, 0.3ms) was delivered into Choksamni for 20 minutes. We measured the analgesic effect of EA with TFL afer intraperitoneal injection of normal saline, WAYl00635, SB216641 and GR125487. Results : TFLs were gradually decreased in CIA as time elapsed after the immunization of arthrogenic collagen and the maximum value was reached from third to fifth week. EA stimulation on ST36 inhibited chronic inflammatory pain induced by CIA. The analgesic effect of EA was inhibited by pretreatment of $5-HT_{1A}$. antagonist (WAYl00635), $5-HT_{1B}$ antagonist (SB216641) and $5-HT_4$ antagonist (GR125487). Conclusion : Electroacupuncture has the analgesic effect on chronic inflammatory pain and its mechanism was mediated by $5-HT_{1A}$, $5-HT_{1B}$ and $5-HT_4$.

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