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논문 기본 정보

자료유형
학술저널
저자정보
김선영 (원광대학교 경혈학교실) 구성태 (원광대학교 경혈학교실) 김경식 (원광대학교 경혈학교실) 손인철 (원광대학교 경혈학교실)
저널정보
경락경혈학회 Korean Journal of Acupuncture Korean journal of acupuncture 제22권 제1호
발행연도
2005.1
수록면
7 - 21 (15page)

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Objectives : In the present study, the effect of electroacupuncture (EA) applied to SI6 and won-rak point on the ankle sprain model was examined. A common source of persistent pain in humans is the lateral ankle sprain. Methods : To model this condition, the rat's right ankle was bent repeatedly, overextending lateral ligaments, for 4 min under enflurane anesthesia. The rat subsequently showed swelling of the ankle and a reduced stepping force of the affected limb for the next several days. The reduced stepping force of the limb was presumably due to a painful ankle. EA was applied to the several acupuncture point on the contralateral forelimb for 30 min under gaseous anesthesia. After the termination of EA, behavioral tests measuring stepping force and Paw volume were Periodically conducted during the next 4 h and 18 h respectively. Results : EA applied to $SI_6$ with won-rak point produced more powerful improvement of stepping force of the sprained foot than to $SI_6$ alone lasting for at least 4 h. However, neigher $KI_4$ point nor $BL_{64}$ point produced any significant increase of weight bearing force. The improvement of stepping pressure was interpreted as an analgesic effect. The analgesic effect was specific to the acupuncture point since the analgesic effort on the ankle sprain pain model could not be mimicked by EA applied to $KI_4$ or $BL_{64}$. In addition, EA applied to $SI_6$ with won-rak combination point showed inhibitory effect on the paw edema induced by ankle sprain. Also, COX-2 protein expression increased by ankle sprain were suppressed by the EA stimulation. Conclusion : These data suggest that EA with won-rak combination point produces a more potent analgesic effect on the ankle sprain pain model in the rat and that EA with won-rak combination point induced anti-inflammatory effect through the suppression of COX-2 protein expression.

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