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The Effects of NEES on PARP Expression and Cell Death in Rat Cerebral Cortex After Ischemic Injury
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  • The Effects of NEES on PARP Expression and Cell Death in Rat Cerebral Cortex After Ischemic Injury
  • The Effects of NEES on PARP Expression and Cell Death in Rat Cerebral Cortex After Ischemic Injury
저자명
Kim. Sung-Won,Lee. Jung-Sook,Um. Ki-Mai,Kim. Ji-Sung,Lee. Suk-Hee,Choi. Yoo-Rim,Kim. Nyeon-Jun,Kim. Bo-Kyoung,Cho. Mi-Suk,Park.
간행물명
Journal of international academy of physical therapy research
권/호정보
2010년|1권 2호|pp.107-112 (6 pages)
발행정보
국제물리치료학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

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.