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저빈도 전침자극이 류마토이드 관절염 유발 흰쥐 대뇌피질 Nicotidamide Adenine Dinucleotide Phosphate-diaphorase(NADPH-d) 양성세포 발현에 미치는 영향
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  • 저빈도 전침자극이 류마토이드 관절염 유발 흰쥐 대뇌피질 Nicotidamide Adenine Dinucleotide Phosphate-diaphorase(NADPH-d) 양성세포 발현에 미치는 영향
저자명
정기훈,노정두,김이화,이은용,Jung. Ki-Hoon,Roh. Jeong-Du,Kim. E-Hwa,Lee. Eun-Yong
간행물명
大韓鍼灸學會誌= The journal of Korean Acupuncture & Moxibustion Society
권/호정보
2008년|25권 3호|pp.179-187 (9 pages)
발행정보
대한침구학회
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Objectives & Methods : This study was to investigate effect of low frequency electroacupuncture on NADPH-d positive neurons in the brain cortex of rat with adjuvant induced rheumatoid arthritis. Experimental groups were divided into 6 groups ; Normal, Control, $ST_{36}$, $SP_9$, $ST_{36}+SP_9$ and Non-Acupoint. Normal group, non-arthritic group, was injected normal saline, and the other groups were injected FCA. Each acupoint groups were treated by 2Hz electroacupuncture at each acupoints and NA group was treated by 2Hz electroacupuncture at non-acupoint. Each groups were evaluated by the number of NADPH-d positive neurons in primary somatosensory area(S1), secondary somatosensory area(S2), motor area and caudate putamen by using an image analyzer and a microscope. Results : 1. In S1, the number of NADPH-d positive neuron cells in the $ST_{36}$ group were significantly(p<0.05) increased compared with the control group. 2. In S2, the number of NADPH-d positive neuron cells in all electroacupuncture groups were not significantly changed compared with the control group. 3. In motor area, the number of NADPH-d positive neuron cells in $ST_{36}$ group, $SP_9$ group, NA group were significantly(p<0.05) increased compared with the control group. 4. In Caudate putamen, the number NADPH-d positive neuron cells in all electroacupuncture groups were significantly(p<0.05) decreased compared with the control group. Conclusions : Our result demonstrated that low frequency electroacupuncture on $ST_{36}$ & $SP_9$ normalized expression of NADPH-d positive neurons in the brain cortex of the rheumatoid arthritis model in rats.