본문 바로가기
KERD
논문KCI 등재

공진단이 MCAO모델 흰쥐에서 gliosis 억제에 미치는 영향

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

2

조회

0

다운로드

9

인용

0

참고문헌

키워드

주제분류한의학

초록

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.

Abstract

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.

참고문헌 (43)

  1. Broude E, "Fetal spinal cord transplants and exogenous neurotrophic support enhance c-Jun expression in mature axotomized neurong after spinal cord injury", Exp Nerol, 155, pp.439~455 (1999)
  2. Eng LF, "Astrocyte activation and fibrou gliosis : Glial fibrillary acidic protein immunostaining of astrocytes following intraspinal cord grafting of fetal CNS tissue", Prog Brain Res, 71, pp.439~455 (1987)
  3. Houle J, "The structural integrity of glial scar tissue associated with a chronic spinal cord lesion can be altered by tansplated fetal spinal cord tissue", J Neurosci Res, 31, pp.120~130 (1992)
  4. Miros Pekny, "Astrocyte activation and reactive gliosis", Glia, 50, pp.427~434 (2005)
  5. Dijkstra S, "Intraspinal administration of an antibody against CD81 enhances functional recovery and tissue sparing after experimental spinal cord injury", Exp Neurol, 202(1), pp.57~66 (2006)
  6. Menet V, "GFAP null astrocytes are a favorable substrate for neuronal survival and neurite growth", Glia, 31(3), pp.267~272 (2000)
  7. 김갑성, "실용동서의학임상총서 3권", pp.22~30 (2001), 도서출판정담
  8. 김영훈, "공진단이 백서의 고지혈증 지질대사에 미치는 영향", 東西醫學, 14(2), pp.61~78 (1989)
  9. 박치상, "拱辰丹의 성분 분석 및 抗酸化 작용에 미치는 영향", 대한본초학회지, 22(2), pp.51~63 (2007), 대한본초학회
  10. 黃善美, "공진단이 CT105와 β-amyloid로 유발된 Alzheimer's disease 病態 모델에 미치는 영향", pp.2004
  11. Longa EZ, "Reversible middle cerebral artery occlusion without craniectomy in rats", Stroke, 20, pp.84~91 (1989)
  12. 김진호, "재활의학", pp.349~353 (2003), 군자출판사
  13. PH Horner, "Regeneratiing the damaged central nervous system", Nature, 409, pp.963~ (2000)
  14. O'Callaghan JP, "Assessment of neurotoxicology -use of glial fivrillary acidic protein as a biomarker", Biomedial and envionmental sciences, 4, pp.197~206 (1991)
  15. O'Callaghan JP, "Assessment of neurotoxic using assays of neurin and glial localized proteins -chronology and critique. Neurotoxicology", pp.83~99 (1992), Ravin Press Ltd
  16. Barres BA, "Ion channels in certebrate glia. Annu Rev", Neurosci, 13, pp.441~474 (1990)
  17. Malhotra S, "Reactive astrocyte-a review", Cytobios, 61, pp.133~160 (1990)
  18. Anderson MF, "Astrocytes and stroke: networking for survival?", Neurochem Res, 28(2), pp.293~305 (2003)
  19. Norenberg MD, "Astrocytes responses to CNS injury", J Neuropathol Exp Neurol, 53, pp.213~220 (1994)
  20. Norenberg MD, "Reactive astrocytosis", the Role of gloa in Neurotoxicity, pp.93~107 (1996)
  21. O'Callaghan JP, "Glucocorticoids regulate the synthesis of glialfibrillary acidic protein in intact and adrenlectomized rats but do not affect its expression following brain injury", J Neurochem, 57, pp.860~869 (1991)
  22. Vijayan VK, "Increase in glial fibrillary acidic protein following neural trauma. Mol. Chem", Neuropathol, 13, pp.107~118 (1990)
  23. Oren R, "Biochem", Biophys Res Com, 222, pp.13~18 (1966)
  24. Dijkstra S, "Up-regulation of CD81(target of the antiproliferative antibody; TAPA) by reactive microglia and astrocytes after spinal cord injury in the rat", J Comp Neurol, 428, pp.266~277 (2000)
  25. Levy S, "CD 81(TAPA-1): a molecule involved in signal transduction and cell adhesion in the immune system", Annu Rev Immunol, 16, pp.89~109 (1998)
  26. Dijkstra S, "CD81 and microglial activation in vitro proliferation, phagocytosis and nitric oxide production", J Neuroimmunol, 114, pp.151~159 (2001)
  27. Koistinaho J, "Differntial expression of small heat shock proteins in reactive astorcytes after focal ischemia: possible role of beta-adrenergic receptor", J Neurosci, 19(22), pp.9768~9779 (1999)
  28. Yamaguchi A, "Stress-Associated endoplasmic retculum protein 1(SERP1)", ribosome -associated membrane protein4(RAMP4) stabilizes membrane proteins during stress and faciliates subsequent glycosylation, 1999, pp.147, 1195~1204
  29. Onodera H, "Proto-oncogene c-fos is transiently induced in the rat cerebral cortex after forebrain ischemia", Neurosci. L.eff, 98(1), pp.101~104 (1989)
  30. Herrera DG, "Activation of c-fos in the brain. Prog", Neurobiol, 50(2-3), pp.83~107 (1996)
  31. Gubits RM, "Immediate-early gene induction after neuronal hypoxiaischemia", Mol Brain Res, 18, pp.228~238 (1993)
  32. Hafezi F, "The absence of c-Fos prevents light induced apoptotic cell death of photoreceptors in retinal degeneration in vivo", Nat Med, 3, pp.346~349 (1997)
  33. Akins PT, "Immediate early gene expression in response to cerebral ischemia: friend or foe?", Stroke, 27, pp.1682~1687 (1996)
  34. Seger R, "The MAPK signaling cascade", FASEB J, 9, pp.726~735 (1995)
  35. Masuhara K, "Involvement of extracellular signal-regulated protein kinase in gliosis induced during recovery from metabolic inhibition", Biochem Biophys Res Commun, 267(3), pp.892~896 (2000)
  36. Bonni A, "Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms", Science, 286, pp.1358~1362 (1999)
  37. Han B, "BDNF protects the neonatal brain from hypoxic-ischemic injury in vivo via the ERK pathway", J Neurosci, 20, pp.5775~5781 (2000)
  38. Namura S, "Intravenous administration of MEK inhibitor U0126 aVords brain protection against forebrain ischemia and focal cerebral ischemia", Proc Natl Acad Sci USA, 98(20), pp.11569~11574 (2001)
  39. 危亦林, "世醫得效方", pp.271~ (1990), 人民衛生出版社
  40. 許浚, "東醫寶鑑(雜病篇)", pp.828~ (2005), 法印文化史
  41. 金定濟, "診療要覽(下)", pp.438~ (1974), 東洋醫學硏究院
  42. 裵元植, "韓方臨床學", pp.820~821 (1986), 南山堂
  43. 김창민, "完譯中藥大辭典", pp.1036~1043 (1998), 도서출판정담

관련 논문AI추천

이 간행물의 다른 논문 (21건)