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    급성 뇌 경색 동물모델에서 Nafamostat의 뇌 손상 억제효과 규명 연구

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    https://www.riss.kr/link?id=T13434331

    • 저자
    • 발행사항

      대전 : 충남대학교 대학원, 2014

    • 학위논문사항

      학위논문(석사) -- 충남대학교 대학원 , 의과학과 의과학 전공 , 2014. 2

    • 발행연도

      2014

    • 작성언어

      한국어

    • DDC

      610 판사항(22)

    • 발행국(도시)

      대전

    • 기타서명

      The effect of nafamostatmesilate(NM) onischemic stroke in middle cerebral artery occlusionmodels
      Effect of nafamostatmesilate(NM) onischemic stroke in middle cerebral artery occlusionmodels

    • 형태사항

      ii, 34 p. : 삽화 ; 26 cm.

    • 일반주기명

      충남대학교 논문은 저작권에 의해 보호받습니다.
      지도교수: 김국성
      참고문헌 : p. 29-32

    • 소장기관
      • 충남대학교 도서관 소장기관정보
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    다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

    Nafamostat mesilate (NM), a serine protease inhibitor, has a broad range of clinical use such as an anticoagulant during hemodialysis for cerebral hemorrhage patients, an agent to improve acute pancreatitis, and a hemoperfusion anticoagulant for patients with intravascular coagulation, hemorrhagic lesion, and hemorrhagic tendency. However, the effect of NM on acute embolic cerebral infarction has not been studied.
    In the present study, NM decreased the size of infarct and brain edema after induction of transient focal ischemia using middle cerebral artery occlusion (MCAO) compared to control. In addition, NM inhibited the increase of motor neurological scoring induced by MCAO. Neuron degeneration is induced in cerebral cortex of MCAO group. Furthermore, the activation of glia cell and astrocyte induced by MCAO group is inhibited in NM treated group. GRP78 was increased in the MCAO group compared with control. However, this increase induced by MCAO is inhibited in NM treated group. Furthermore, CHOP and p-eIF2α were increased in the cerebral cortex of MCAO group. But this increase, also, inhibited in NM treated group.
    These results collectively suggest that NM reduces cerebral injury after MCAO via inhibiting neuron degeneration and ER stress suggesting NM has a neuro-protective effect in ischemic-reperfusion injury.
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    Nafamostat mesilate (NM), a serine protease inhibitor, has a broad range of clinical use such as an anticoagulant during hemodialysis for cerebral hemorrhage patients, an agent to improve acute pancreatitis, and a hemoperfusion anticoagulant for patie...

    Nafamostat mesilate (NM), a serine protease inhibitor, has a broad range of clinical use such as an anticoagulant during hemodialysis for cerebral hemorrhage patients, an agent to improve acute pancreatitis, and a hemoperfusion anticoagulant for patients with intravascular coagulation, hemorrhagic lesion, and hemorrhagic tendency. However, the effect of NM on acute embolic cerebral infarction has not been studied.
    In the present study, NM decreased the size of infarct and brain edema after induction of transient focal ischemia using middle cerebral artery occlusion (MCAO) compared to control. In addition, NM inhibited the increase of motor neurological scoring induced by MCAO. Neuron degeneration is induced in cerebral cortex of MCAO group. Furthermore, the activation of glia cell and astrocyte induced by MCAO group is inhibited in NM treated group. GRP78 was increased in the MCAO group compared with control. However, this increase induced by MCAO is inhibited in NM treated group. Furthermore, CHOP and p-eIF2α were increased in the cerebral cortex of MCAO group. But this increase, also, inhibited in NM treated group.
    These results collectively suggest that NM reduces cerebral injury after MCAO via inhibiting neuron degeneration and ER stress suggesting NM has a neuro-protective effect in ischemic-reperfusion injury.

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    목차 (Table of Contents)

    • Ⅰ. 서론 1
    • Ⅱ. 재료 및 연구 방법 4
    • Ⅲ. 연구결과 9
    • Ⅳ. 고찰 24
    • Ⅴ. 결론 27
    • Ⅰ. 서론 1
    • Ⅱ. 재료 및 연구 방법 4
    • Ⅲ. 연구결과 9
    • Ⅳ. 고찰 24
    • Ⅴ. 결론 27
    • Ⅵ. 참고문헌 29
    • ABSTRACT 33
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