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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2009.1
- 수록면
- 674 - 684 (11page)
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초록· 키워드
오류제보하기
Objectives : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis becomes physical and a mechanical barrier to axonal regeneration. Reactive gliosis induced by ischemic injury such as middle cerebral artery occlusion is involved with up-regulation of GFAP and CD81. The current study was to examine the effect of the Gongjin-dan (GJD) on CD81 and GFAP expression and its pathway in the rat brain following middle cerebral artery occlusion (MCAO).
Methods : In order to study ischemic injuries on the brain, infarction was induced by MCAO using insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. Cresyl violet staining, cerebral infarction size measurement, immunohistochemistry and microscopic examination were used to detect the expression of CD81 and GFAP and the effect on the infarct size and pyramidal cell death in the brain of the rat with cerebral infarction induced by MCAO. Also, c-Fos and ERK expression was measured to investigate the signaling pathway after GJD administration in MCAO rats.
Results : The following results were obtained:
Measuring the size of cerebral infarction induced by MCAO in the rat after injection of GJD showed the size was decreased. GJD administration showed pyramidal cell death protection in the hippocampus in the MCAO rat. GJD administration decreased GFAP expression in the MCAO rat. GJD administration decreased CD81 expression in the MCAO rat. GJD administration induced up-regulation of c-FOS expression compared with MCAO. GJD administration induced down-regulation of ERK expression compared with MCAO.
Conclusion : We observed that GJD could suppress the reactive gliosis, which disturbs the axonal regeneration in the brain of the rat with cerebral infarction after MCAO by controlling the expression of CD81 and GFAP. The effect may be modulated by the regulation of c-Fos and ERK. These results suggest that GJD can be a candidate to regenerate CNS injury.
목차
등록된 정보가 없습니다.
참고문헌 (28)
참고문헌 신청
Anderson MF / 2003 / Astrocytes and stroke: networking for survival? / Neurochem Res 28 (2) : 293 ~ 305
Barres BA / 1990 / Ion channels in certebrate glia. Annu Rev / Neurosci 13 : 441 ~ 474
Broude E / 1999 / Fetal spinal cord transplants and exogenous neurotrophic support enhance c-Jun expression in mature axotomized neurong after spinal cord injury / Exp Nerol
Dijkstra S / 2000 / Up-regulation of CD81(target of the antiproliferative antibody; TAPA) by reactive microglia and astrocytes after spinal cord injury in the rat / J Comp N
Dijkstra S / 2001 / CD81 and microglial activation in vitro proliferation, phagocytosis and nitric oxide production / J Neuroimmunol 114 : 151 ~ 159
Barres BA / 1990 / Ion channels in certebrate glia. Annu Rev / Neurosci 13 : 441 ~ 474
Broude E / 1999 / Fetal spinal cord transplants and exogenous neurotrophic support enhance c-Jun expression in mature axotomized neurong after spinal cord injury / Exp Nerol
Dijkstra S / 2000 / Up-regulation of CD81(target of the antiproliferative antibody; TAPA) by reactive microglia and astrocytes after spinal cord injury in the rat / J Comp N
Dijkstra S / 2001 / CD81 and microglial activation in vitro proliferation, phagocytosis and nitric oxide production / J Neuroimmunol 114 : 151 ~ 159
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