中华物理医学与康复杂志
中華物理醫學與康複雜誌
중화물리의학여강복잡지
CHINESE JOURNAL OF PHYSICAL MEDICINE AND REHABILITATION
2014年
7期
508-511
,共4页
杨杰华%冼晓琪%区大明%孙静
楊傑華%冼曉琪%區大明%孫靜
양걸화%승효기%구대명%손정
高压氧%尼膜同%脑小血管病%脑源性神经生长因子%乙酰胆碱%学习记忆
高壓氧%尼膜同%腦小血管病%腦源性神經生長因子%乙酰膽堿%學習記憶
고압양%니막동%뇌소혈관병%뇌원성신경생장인자%을선담감%학습기억
Hyperbaric oxygen%Nimotop%Cerebral small vessel disease%Brain-derived neurotrophic factors%Acetylcholine%Learning%Memory
目的 观察高压氧治疗对脑小血管病(CSVD)模型大鼠脑皮质及海马区脑源性神经生长因子(BDNF)及乙酰胆碱(Ach)表达的影响,同时观察治疗前、后大鼠学习记忆功能改善情况,并探讨高压氧治疗CSVD的可能机制.方法 选取健康雄性Wistar大鼠60只,采用颈外动脉注射粒径为48 ~ 74 μm大鼠同种异体血栓制成CSVD大鼠模型.选用随机数字表法将上述CSVD模型大鼠分为高压氧组、尼膜同组及对照组.高压氧组大鼠于制模12h后给予高压氧治疗,尼膜同组大鼠于制模12h后给予尼膜地平片-混悬液灌胃,对照组大鼠制模后不给予任何特殊干预.各组大鼠分别于制模7d、14d及28 d时通过Morris水迷宫实验观察其学习记忆功能改变;于制模28 d时采用酶联免疫吸附法(ELISA)检测各组大鼠脑皮质及海马区BDNF、Ach含量.结果 制模14 d、28 d时高压氧组大鼠逃避潜伏期[分别为(28.5±6.6)s和(15.8±4.7)s]均显著短于尼膜同组及对照组(P<0.05),穿越平台次数[分别为(3.4±1.2)次/分钟和(4.5±1.9)次/分钟]均较尼膜同组及对照组明显增多(P<0.05);另外制模14 d、28 d时尼膜同组逃避潜伏期及穿越平台次数亦显著优于对照组(P<0.05).高压氧组大鼠脑皮质、海马中Ach含量[分别为(175.1±23.5) μg/g和(158.8±25.5) μg/g]及BDNF含量[分别为(105.1 ±7.9) μg/g和(172.1 ±23.1) μg/g]均较尼膜同组和对照组明显增多(P<0.05);尼膜同组脑皮质、海马部位Ach及BDNF含量亦较对照组明显增多(P<0.05).结论 高压氧干预能促进CSVD大鼠BDNF释放,有助于保护及修复神经元线粒体,维持脑皮质及海马区神经递质Ach处于稳定水平,对改善大鼠学习、记忆功能具有重要作用,其疗效优于尼膜同药物治疗.
目的 觀察高壓氧治療對腦小血管病(CSVD)模型大鼠腦皮質及海馬區腦源性神經生長因子(BDNF)及乙酰膽堿(Ach)錶達的影響,同時觀察治療前、後大鼠學習記憶功能改善情況,併探討高壓氧治療CSVD的可能機製.方法 選取健康雄性Wistar大鼠60隻,採用頸外動脈註射粒徑為48 ~ 74 μm大鼠同種異體血栓製成CSVD大鼠模型.選用隨機數字錶法將上述CSVD模型大鼠分為高壓氧組、尼膜同組及對照組.高壓氧組大鼠于製模12h後給予高壓氧治療,尼膜同組大鼠于製模12h後給予尼膜地平片-混懸液灌胃,對照組大鼠製模後不給予任何特殊榦預.各組大鼠分彆于製模7d、14d及28 d時通過Morris水迷宮實驗觀察其學習記憶功能改變;于製模28 d時採用酶聯免疫吸附法(ELISA)檢測各組大鼠腦皮質及海馬區BDNF、Ach含量.結果 製模14 d、28 d時高壓氧組大鼠逃避潛伏期[分彆為(28.5±6.6)s和(15.8±4.7)s]均顯著短于尼膜同組及對照組(P<0.05),穿越平檯次數[分彆為(3.4±1.2)次/分鐘和(4.5±1.9)次/分鐘]均較尼膜同組及對照組明顯增多(P<0.05);另外製模14 d、28 d時尼膜同組逃避潛伏期及穿越平檯次數亦顯著優于對照組(P<0.05).高壓氧組大鼠腦皮質、海馬中Ach含量[分彆為(175.1±23.5) μg/g和(158.8±25.5) μg/g]及BDNF含量[分彆為(105.1 ±7.9) μg/g和(172.1 ±23.1) μg/g]均較尼膜同組和對照組明顯增多(P<0.05);尼膜同組腦皮質、海馬部位Ach及BDNF含量亦較對照組明顯增多(P<0.05).結論 高壓氧榦預能促進CSVD大鼠BDNF釋放,有助于保護及脩複神經元線粒體,維持腦皮質及海馬區神經遞質Ach處于穩定水平,對改善大鼠學習、記憶功能具有重要作用,其療效優于尼膜同藥物治療.
목적 관찰고압양치료대뇌소혈관병(CSVD)모형대서뇌피질급해마구뇌원성신경생장인자(BDNF)급을선담감(Ach)표체적영향,동시관찰치료전、후대서학습기억공능개선정황,병탐토고압양치료CSVD적가능궤제.방법 선취건강웅성Wistar대서60지,채용경외동맥주사립경위48 ~ 74 μm대서동충이체혈전제성CSVD대서모형.선용수궤수자표법장상술CSVD모형대서분위고압양조、니막동조급대조조.고압양조대서우제모12h후급여고압양치료,니막동조대서우제모12h후급여니막지평편-혼현액관위,대조조대서제모후불급여임하특수간예.각조대서분별우제모7d、14d급28 d시통과Morris수미궁실험관찰기학습기억공능개변;우제모28 d시채용매련면역흡부법(ELISA)검측각조대서뇌피질급해마구BDNF、Ach함량.결과 제모14 d、28 d시고압양조대서도피잠복기[분별위(28.5±6.6)s화(15.8±4.7)s]균현저단우니막동조급대조조(P<0.05),천월평태차수[분별위(3.4±1.2)차/분종화(4.5±1.9)차/분종]균교니막동조급대조조명현증다(P<0.05);령외제모14 d、28 d시니막동조도피잠복기급천월평태차수역현저우우대조조(P<0.05).고압양조대서뇌피질、해마중Ach함량[분별위(175.1±23.5) μg/g화(158.8±25.5) μg/g]급BDNF함량[분별위(105.1 ±7.9) μg/g화(172.1 ±23.1) μg/g]균교니막동조화대조조명현증다(P<0.05);니막동조뇌피질、해마부위Ach급BDNF함량역교대조조명현증다(P<0.05).결론 고압양간예능촉진CSVD대서BDNF석방,유조우보호급수복신경원선립체,유지뇌피질급해마구신경체질Ach처우은정수평,대개선대서학습、기억공능구유중요작용,기료효우우니막동약물치료.
Objective To observe the effects of hyperbaric oxygen (HBO) on cerebral small vessel disease (CSVD) and on learning,memory and the expression of brain-derived neurotrophic factor (BDNF) and acetylcholine (Ach) in the cerebral cortex and hippocampus.Methods Sixty healthy,male Wistar rats were studied.Allograft thrombosis particles 48 to 74 μm in diameter were injected into the rats' external carotid arteries to create a CSVD model.The rats were then divided randomly into a hyperbaric oxygen group,a nimotop group and a control group.The hyperbaric oxygen group rats were given hyperbaric oxygen therapy 12 hours after the modeling.The nimotop group rats were given nimodipine by intragastric perfusion 12h after the modeling.The rats in the control group had no special intervention.At 7,14 and 28 days after the modeling,any changes in learning and memory were assessed with a Morris water maze test.Enzyme-linked immunosorbent assay (ELISA) was used to detect the expression of BDNF in the cerebral cortex and of Ach in the hippocampus at 28 days.Results At both 14 and 28 days the average escape latency of the rats in the hyperbaric oxygen group was significantly shorter than those of the nimotop and control groups.The average platform crossing time had increased significantly more than in the nimotop and control groups.At both 14 and 28 days the escape latency and platform crossing times of the nimotop group were significantly better than in the control group.Ach content and BDNF content were significantly higher in the HBO group than in the nimotop and control groups.Conclusions Hyperbaric oxygen treatment can promote BDNF release in CSVD,which is helpful to protect and repair neural mitochondria,to maintain the cortex and hippocampal neurotransmitters on a stable level,and to improve learning and memory.Its effect is better than that of nimotop.