中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2010年
4期
721-724
,共4页
卢舜飞%孙丽娜%沈佳%苏方%王会平%叶治国%叶挺梅%夏强
盧舜飛%孫麗娜%瀋佳%囌方%王會平%葉治國%葉挺梅%夏彊
로순비%손려나%침가%소방%왕회평%협치국%협정매%하강
黑木耳多糖%脑缺血%Morris水迷宫%丙二醛%超氧化物歧化酶
黑木耳多糖%腦缺血%Morris水迷宮%丙二醛%超氧化物歧化酶
흑목이다당%뇌결혈%Morris수미궁%병이철%초양화물기화매
Auricularia auricular polysaccharide%Brain ischemia%Morris water maze%Malondialdehyde%Superoxide dismutase
目的:观察黑木耳多糖(AAP)对大鼠慢性脑缺血损伤的保护作用,并探讨其相关机制.方法:雄性成年SD大鼠右侧永久性大脑中动脉栓塞(MCAO),建立慢性脑缺血模型,缺血后每天分别给予不同浓度的AAP灌胃4周.银杏叶提取物作为阳性对照.4周后采用Morris水迷宫检测大鼠学习记忆能力.取脑做冰冻切片进行Nissl染色,观察存活神经元数量,并测定脑组织丙二醛(MDA)水平和超氧化物歧化酶(SOD)活性.结果:AAP能明显改善脑缺血大鼠的学习记忆能力,增加海马神经元的存活数量,并且能够使脑组织长期MCAO诱导的MDA生成减少,使SOD活性显著升高.高剂量AAP(200 mg/kg)的作用和银杏叶提取物相比更明显.结论:AAP明显减轻大鼠慢性脑缺血损伤,其作用与其对抗过氧化应激有关.
目的:觀察黑木耳多糖(AAP)對大鼠慢性腦缺血損傷的保護作用,併探討其相關機製.方法:雄性成年SD大鼠右側永久性大腦中動脈栓塞(MCAO),建立慢性腦缺血模型,缺血後每天分彆給予不同濃度的AAP灌胃4週.銀杏葉提取物作為暘性對照.4週後採用Morris水迷宮檢測大鼠學習記憶能力.取腦做冰凍切片進行Nissl染色,觀察存活神經元數量,併測定腦組織丙二醛(MDA)水平和超氧化物歧化酶(SOD)活性.結果:AAP能明顯改善腦缺血大鼠的學習記憶能力,增加海馬神經元的存活數量,併且能夠使腦組織長期MCAO誘導的MDA生成減少,使SOD活性顯著升高.高劑量AAP(200 mg/kg)的作用和銀杏葉提取物相比更明顯.結論:AAP明顯減輕大鼠慢性腦缺血損傷,其作用與其對抗過氧化應激有關.
목적:관찰흑목이다당(AAP)대대서만성뇌결혈손상적보호작용,병탐토기상관궤제.방법:웅성성년SD대서우측영구성대뇌중동맥전새(MCAO),건립만성뇌결혈모형,결혈후매천분별급여불동농도적AAP관위4주.은행협제취물작위양성대조.4주후채용Morris수미궁검측대서학습기억능력.취뇌주빙동절편진행Nissl염색,관찰존활신경원수량,병측정뇌조직병이철(MDA)수평화초양화물기화매(SOD)활성.결과:AAP능명현개선뇌결혈대서적학습기억능력,증가해마신경원적존활수량,병차능구사뇌조직장기MCAO유도적MDA생성감소,사SOD활성현저승고.고제량AAP(200 mg/kg)적작용화은행협제취물상비경명현.결론:AAP명현감경대서만성뇌결혈손상,기작용여기대항과양화응격유관.
AIM: To investigate the effects of auricularia auricular polysaccharide (AAP) on chronic cerebral ischemia injury in rats. METHODS: The chronic cerebral ischemia mode1 was made by permanent middle cerebral artery occlusion (MCAO) on the right side. AAP at different doses (50 mg/kg and 100 mg/kg) was intragastrically administered at the onset of ischemia and in the following days after operation, once a day for 4 weeks. After 4 weeks of MCAO, Morris water maze test was introduced to examine the learning and memory functions. Nissl staining was performed to detect the survival neurons in hippocampal slices. Level of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in brain tissue were measured. RESULTS: Rats treated with AAP showed a shorter escaping latency in spacial navigation test because the AAP treated rats spent less time to find the platform in spatial probe test. More survival neurons in hippocampal slices were observed from AAP treated rats. Also, the MDA level in brain tissue was reduced and SOD activity in brain tissue was increased in the AAP treated rats with MCAO. CONCLUSION: AAP protects rats from chronic brain ischemic injury, in which its anti-oxidative effect might be involved.