中华神经科杂志
中華神經科雜誌
중화신경과잡지
Chinese Journal of Neurology
2012年
6期
421-424
,共4页
田利丽%郭芮兵%王兆露%吕秋石%黄显军%徐格林%刘新峰
田利麗%郭芮兵%王兆露%呂鞦石%黃顯軍%徐格林%劉新峰
전리려%곽예병%왕조로%려추석%황현군%서격림%류신봉
脑损伤%淀粉样B蛋白前体%神经生长因子%投药,鼻内%大鼠
腦損傷%澱粉樣B蛋白前體%神經生長因子%投藥,鼻內%大鼠
뇌손상%정분양B단백전체%신경생장인자%투약,비내%대서
Brain injuries%Amyloid beta-peptide%Nerve growth factor%Administration,intranasal%Rats
目的 探讨经鼻给神经生长因子(NGF)对实验性创伤性脑损伤(TBI)大鼠中枢神经系统中β-淀粉样蛋白(Aβ)表达的影响.方法 将80只大鼠采用完全随机分组法分为假手术组(n=26)、对照组(n=27)和治疗组(n=27),参照Feeney自由落体法制作TBI大鼠模型,治疗组经鼻给予NGF治疗.采用平衡木和Morris水迷宫方法评估3组大鼠的神经功能恢复情况.取伤侧海马,通过ELISA方法定量各组大鼠海马部位Aβ的表达;行免疫组织化学染色检测各组大鼠脑组织中淀粉样蛋白前体(APP)的生成情况.结果 治疗组TBI大鼠与对照组相比,平衡木运动协调功能(s)恢复较快(19.00±6.99与27.33±7.39,F2,b=12.87,P=0.028),Morris水迷宫实验显示治疗组潜伏期明显短于对照组;治疗组在原平台象限所占时间百分比(45.82%±11.15%)及穿越平台次数(8.60±2.73)较对照组(33.99%±3.46%、3.60±2.06)均明显增多(F2,15=6.814,P=0.037;F2,15=5.346,P=0.04).ELISA检测显示治疗组Aβ浓度的增高幅度较对照组下降显著.免疫组织化学观察发现APP的阳性细胞数目在3组之间差异有统计学意义(F2,15=8.672,P=O.O03),但对照组和治疗组相比差异无统计学意义.结论 经鼻给NGF可降低TBI大鼠中枢神经系统中Aβ的表达,促进损伤后神经功能的恢复.
目的 探討經鼻給神經生長因子(NGF)對實驗性創傷性腦損傷(TBI)大鼠中樞神經繫統中β-澱粉樣蛋白(Aβ)錶達的影響.方法 將80隻大鼠採用完全隨機分組法分為假手術組(n=26)、對照組(n=27)和治療組(n=27),參照Feeney自由落體法製作TBI大鼠模型,治療組經鼻給予NGF治療.採用平衡木和Morris水迷宮方法評估3組大鼠的神經功能恢複情況.取傷側海馬,通過ELISA方法定量各組大鼠海馬部位Aβ的錶達;行免疫組織化學染色檢測各組大鼠腦組織中澱粉樣蛋白前體(APP)的生成情況.結果 治療組TBI大鼠與對照組相比,平衡木運動協調功能(s)恢複較快(19.00±6.99與27.33±7.39,F2,b=12.87,P=0.028),Morris水迷宮實驗顯示治療組潛伏期明顯短于對照組;治療組在原平檯象限所佔時間百分比(45.82%±11.15%)及穿越平檯次數(8.60±2.73)較對照組(33.99%±3.46%、3.60±2.06)均明顯增多(F2,15=6.814,P=0.037;F2,15=5.346,P=0.04).ELISA檢測顯示治療組Aβ濃度的增高幅度較對照組下降顯著.免疫組織化學觀察髮現APP的暘性細胞數目在3組之間差異有統計學意義(F2,15=8.672,P=O.O03),但對照組和治療組相比差異無統計學意義.結論 經鼻給NGF可降低TBI大鼠中樞神經繫統中Aβ的錶達,促進損傷後神經功能的恢複.
목적 탐토경비급신경생장인자(NGF)대실험성창상성뇌손상(TBI)대서중추신경계통중β-정분양단백(Aβ)표체적영향.방법 장80지대서채용완전수궤분조법분위가수술조(n=26)、대조조(n=27)화치료조(n=27),삼조Feeney자유락체법제작TBI대서모형,치료조경비급여NGF치료.채용평형목화Morris수미궁방법평고3조대서적신경공능회복정황.취상측해마,통과ELISA방법정량각조대서해마부위Aβ적표체;행면역조직화학염색검측각조대서뇌조직중정분양단백전체(APP)적생성정황.결과 치료조TBI대서여대조조상비,평형목운동협조공능(s)회복교쾌(19.00±6.99여27.33±7.39,F2,b=12.87,P=0.028),Morris수미궁실험현시치료조잠복기명현단우대조조;치료조재원평태상한소점시간백분비(45.82%±11.15%)급천월평태차수(8.60±2.73)교대조조(33.99%±3.46%、3.60±2.06)균명현증다(F2,15=6.814,P=0.037;F2,15=5.346,P=0.04).ELISA검측현시치료조Aβ농도적증고폭도교대조조하강현저.면역조직화학관찰발현APP적양성세포수목재3조지간차이유통계학의의(F2,15=8.672,P=O.O03),단대조조화치료조상비차이무통계학의의.결론 경비급NGF가강저TBI대서중추신경계통중Aβ적표체,촉진손상후신경공능적회복.
Objective To study the effect of intranasal nerve growth factor (NGF) on the expression of amyloid-β,peptide (Aβ) in the central nervous system in rats with traumatic brain injury (TBI).Methods Eighty rats were randomly divided into sham(n =26),control(n =27) and treatment group (n =27 ).They were subjected to the modified Feeney' s weight-drop model.The treatment group was treated with NGF administered by nasal route,and the control group was given phosphate-buffered saline (PBS).Beam walking and Morris water maze test were performed in the three groups.The concentration of Aβ40 and Aβ42 in the injured ipsilateral hippocampus was elevated by ELISA measurement.Immunohistochemistry was used to detect the amyloid precursor protein (APP) positive cells near the region of injury in the hippocampus in rats after TBI.Results NGF group traversed the beam significantly quicker (s) than control group ( 19.00 + 6.99 vs 27.33 ± 7.39 respectively,F2,15 =12.87,P =0.028 ).Morris water maze performance revealed that mean time of latency in the NGF group was significant shorter than vehicle group,and significant memory retention in NGF group as evidenced by a greater percentage of the 60 s allotted time spent in the target quadrant (45.82% ± 11.15% vs 33.99% ± 3.46%,F2,15 =6.814,P=0.037),as well as the number crossing of the former site of the removed platform in NGF group was significant more than control group (8.60 ±2.73 vs 3.60 ±2.06,F2,15 =5.346,P =0.04).The Aβ42 level in control group was increased significantly higher than NGF group as indicated by ELISA measurements.While the Aβ40 level did not have similar shown.Immunohistochemical staining showed that APP level had significant differences among three groups ( F2,15 =8.672,P =0.003).The APP level in NGF group did not alter with control group.Conclusion Intranasal administration of NGF can regulate Aβ42 overproduction,improve the motor and cognitive function after brain injury in rats.