中华结核和呼吸杂志
中華結覈和呼吸雜誌
중화결핵화호흡잡지
Chinese Journal of Tuberculosis and Respiratory Diseases
2012年
1期
24-28
,共5页
王红阳%韩晓庆%赵雅宁%张盼盼%杨林%雷军旗%陈宝元
王紅暘%韓曉慶%趙雅寧%張盼盼%楊林%雷軍旂%陳寶元
왕홍양%한효경%조아저%장반반%양림%뢰군기%진보원
氧化应激%学习记忆%Morris水迷宫%超微结构
氧化應激%學習記憶%Morris水迷宮%超微結構
양화응격%학습기억%Morris수미궁%초미결구
Intermittent hypoxia%Oxidative stress%Function of learning and memory Morris water maze%Ultra microstructure
目的 通过建立重度间歇低氧动物模型,探讨OSAHS大鼠学习记忆功能与氧化应激的关系.方法 成年雄性Wistar大鼠48只,体重(170±10)g,采用随机数字法分为5%间歇性低氧组和对照组,每组又分为2、4、6和8周时间组,每组6只,其中实验组给予5%间歇低氧,并分别在2、4、6、8周进行Morris水迷宫检测学习记忆功能,随后处死大鼠,取脑组织于透射电子显微镜下观察海马区超微结构的变化,通过化学比色法测定海马组织超氧化物歧化酶(SOD)活性和丙二醛水平.结果 与对照组比较,实验组大鼠水迷宫测试大鼠逃避潜伏期时间延长、跨越目标象限时间缩短、穿台次数减少,与对照组相比差异具有统计学意义(P<0.05);随着间歇低氧持续时间延长,实验组各时间点学习功能的改变差异组间比较差异均有统计学意义(均P<0.05).对照组大鼠海马组织于电子显微镜下神经元结构完整,细胞器丰富,而实验组大鼠海马组织的神经元和突触数量明显减少,细胞核皱缩,突触结构模糊,突触间隙增宽,且随着暴露时间的延长,细胞损伤改变愈加明显.与对照组比较,实验组海马组织丙二醛含量明显增高,而SOD活性降低,且随间歇低氧时间延长其变化更为明显,差异有统计学意义(均P<0.05).结论 间歇重度低氧大鼠海马组织存在氧化应激损伤,可能通过引起神经元及突触数量与结构的改变,从而导致学习记忆功能障碍,且随着缺氧时间的延长逐渐加重.
目的 通過建立重度間歇低氧動物模型,探討OSAHS大鼠學習記憶功能與氧化應激的關繫.方法 成年雄性Wistar大鼠48隻,體重(170±10)g,採用隨機數字法分為5%間歇性低氧組和對照組,每組又分為2、4、6和8週時間組,每組6隻,其中實驗組給予5%間歇低氧,併分彆在2、4、6、8週進行Morris水迷宮檢測學習記憶功能,隨後處死大鼠,取腦組織于透射電子顯微鏡下觀察海馬區超微結構的變化,通過化學比色法測定海馬組織超氧化物歧化酶(SOD)活性和丙二醛水平.結果 與對照組比較,實驗組大鼠水迷宮測試大鼠逃避潛伏期時間延長、跨越目標象限時間縮短、穿檯次數減少,與對照組相比差異具有統計學意義(P<0.05);隨著間歇低氧持續時間延長,實驗組各時間點學習功能的改變差異組間比較差異均有統計學意義(均P<0.05).對照組大鼠海馬組織于電子顯微鏡下神經元結構完整,細胞器豐富,而實驗組大鼠海馬組織的神經元和突觸數量明顯減少,細胞覈皺縮,突觸結構模糊,突觸間隙增寬,且隨著暴露時間的延長,細胞損傷改變愈加明顯.與對照組比較,實驗組海馬組織丙二醛含量明顯增高,而SOD活性降低,且隨間歇低氧時間延長其變化更為明顯,差異有統計學意義(均P<0.05).結論 間歇重度低氧大鼠海馬組織存在氧化應激損傷,可能通過引起神經元及突觸數量與結構的改變,從而導緻學習記憶功能障礙,且隨著缺氧時間的延長逐漸加重.
목적 통과건립중도간헐저양동물모형,탐토OSAHS대서학습기억공능여양화응격적관계.방법 성년웅성Wistar대서48지,체중(170±10)g,채용수궤수자법분위5%간헐성저양조화대조조,매조우분위2、4、6화8주시간조,매조6지,기중실험조급여5%간헐저양,병분별재2、4、6、8주진행Morris수미궁검측학습기억공능,수후처사대서,취뇌조직우투사전자현미경하관찰해마구초미결구적변화,통과화학비색법측정해마조직초양화물기화매(SOD)활성화병이철수평.결과 여대조조비교,실험조대서수미궁측시대서도피잠복기시간연장、과월목표상한시간축단、천태차수감소,여대조조상비차이구유통계학의의(P<0.05);수착간헐저양지속시간연장,실험조각시간점학습공능적개변차이조간비교차이균유통계학의의(균P<0.05).대조조대서해마조직우전자현미경하신경원결구완정,세포기봉부,이실험조대서해마조직적신경원화돌촉수량명현감소,세포핵추축,돌촉결구모호,돌촉간극증관,차수착폭로시간적연장,세포손상개변유가명현.여대조조비교,실험조해마조직병이철함량명현증고,이SOD활성강저,차수간헐저양시간연장기변화경위명현,차이유통계학의의(균P<0.05).결론 간헐중도저양대서해마조직존재양화응격손상,가능통과인기신경원급돌촉수량여결구적개변,종이도치학습기억공능장애,차수착결양시간적연장축점가중.
Objective To observe the relations between learning memory function and oxidative stress in rats exposed to severe intermittent hypoxia (IH).Methods Adult male Wistar rats (n =48)were randomly assigned to 2 groups: untreated control group (UC) and 5% intermittent hypoxia group (5% IH).At 2,4,6 and 8 weeks,the learning and memory ability of the rats in each group were assessed with the Morris water maze (MWM) test.The ultrastructural changes in the hippocampus of the rats were observed with transmission electron microscopy (TEM).The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by colorimetric method.Results The water maze test showed that the rats in the 5% IH group had prolonged latency in escaping,reduced target quadrant time in crossing and reduced frequency of crossing the platform,as compared to the UC group (P < 0.05).With longer time of hypoxia,the damage became more significant.It was observed that the structure of neuron cell was complete and organelles were abundant in UC groups.With the extention of exposure time,the number of hippocampus neurons and synaptic were decreased in 5% IH groups,nucleus shrank,synaptic frame became indefinite and synaptic cleft widen.Comparing with control group,the level of MDA in the hippocampal region group was significantly higher (P <0.05) and the activity of SOD significantly was lower (P <0.05) in 5% IH,along with the time expand,which aggravated.Conclusion Severe intermittent hypoxia that results in learning and memory dysfunction.It is possible that oxidative stress change the quantity and structure of hippocampal neurons and synaptic,which aggravates along with the intermittent low oxygen time expand.