대한한방내과학회지 (The Journal of Internal Korean Medicine)

대한한방내과학회 (The Society of Internal Korean Medicine)
권호 표지

공진단이 MCAO모델 흰쥐에서 gliosis 억제에 마치는 영향

The Effect of Gongjin-dan on Gliosis in Middle Cerebral Artery Occlusion (MCAO) Rats

  • 성기문 (원광대학교 한의과대학 내과학교실) ;
  • 허래경 (원광대학교 한의과대학 내과학교실) ;
  • 송봉곤 (원광대학교 한의과대학 내과학교실)
  • Seong, Kee-Moon (Dept. of Oriental Medicine, Won-Kwang University, College of Oriental Medicine) ;
  • Hae, Rae-Kyong (Dept. of Oriental Medicine, Won-Kwang University, College of Oriental Medicine) ;
  • Song, Bong-Keun (Dept. of Oriental Medicine, Won-Kwang University, College of Oriental Medicine)
  • 발행 : 2009.12.30
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초록

Objectives : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis becomes a 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. This study was undertaken 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 were measured to investigate the signaling pathway after GJD administration in MCAO rats. Results : Measuring the size of cerebral infarction induced by MCAO in the rat after injection of GJD showed the size had decreased. GJD administration showed pyramidal cell death protection in the hippocampus in the MCAO rat. GJD administration decreased GF AP 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 a 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.

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