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논문 기본 정보

자료유형
학술저널
저자정보
Kim, Sung-Won (Dongnam Health University) Lee, Jung-Sook (Dongju College) Um, Ki-Mai (Yeoju College) Kim, Ji-Sung (Suwon Women's College) Lee, Suk-Hee (Changwon College) Choi, Yoo-Rim (Daegu Science College) Kim, Nyeon-Jun (Pohang College) Kim, Bo-Kyoung (International University of Korea) Cho, Mi-Suk (Nazarene University) Park, Joo-Hyun (Sarang Hospital) Kim, Soon-Hee (Yongin University)
저널정보
국제물리치료연구학회 Journal of international academy of physical therapy research Journal of international academy of physical therapy research 제1권 제2호
발행연도
2010.1
수록면
107 - 112 (6page)

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The majority of strokes are caused by ischemia and result in brain tissue damage, leading to problems of the central nervous system including hemiparesis, dysfunction of language and consciousness, and dysfunction of perception. The purpose of this study was to investigate the effects of Poly(ADP-ribose) polymerase(PARP) on necrosis in neuronal cells that have undergone needle electrode electrical stimulation(NEES) prior to induction of ischemia. Ischemia was induced in male SD rats(body weight 300g) by occlusion of the common carotid artery for 5 min, after which the blood was reperfused. After induction of brain ischemia, NEES was applied to Zusanli(ST 36), at 12, 24 and 48 hours. Protein expression was investigated using immuno-reactive cells, which react to PARP antibodies in cerebral nerve cells, and Western blotting. The results were as follows: In the cerebral cortex, the number of PARP reactive cells after 24 hours significantly decreased(p<.05) in the NEES group compared to the GI group. PARP expression after 24 hours significantly decreased(p<.05) in the NEES group compared to the GI group. As a result, NEES showed the greatest effect on necrosis-related PARP immuno-reactive cells 24 hours after ischemia, indicating necrosis inhibition, blocking of neural cell death, and protection of neural cells. Based on the results of this study, NEES can be an effective method of treating dysfunction and improving function of neuronal cells in brain damage caused by ischemia.

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