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
2012年
1期
2-7
,共6页
王强%王佩佩%孟萍萍%岳寿伟
王彊%王珮珮%孟萍萍%嶽壽偉
왕강%왕패패%맹평평%악수위
脑缺血再灌注%强化训练%臂板蛋白3A%神经纤毛蛋白-1%细胞凋亡
腦缺血再灌註%彊化訓練%臂闆蛋白3A%神經纖毛蛋白-1%細胞凋亡
뇌결혈재관주%강화훈련%비판단백3A%신경섬모단백-1%세포조망
Cerebral ischemia-reperfusion%Intensive training%Senaphorin 3 A%Neuropilin-1%Cell apoptosis
目的 观察不同强度运动训练对脑缺血再灌注大鼠脑内臂板蛋白3A(Sema3A)及其受体神经纤毛蛋白-1(NP-1)的表达以及缺血侧脑细胞凋亡的影响,探讨强化运动训练促进脑缺血再灌注大鼠运动功能恢复的可能机制.方法 采用线栓法建立左侧大脑中动脉阻塞( MCAO)2 h再灌注动物模型.60只造模成功的雄性Wistar大鼠按随机数字表法分为训练1组、训练2组、训练3组、对照组(各15只鼠).训练1组大鼠每天游泳1次,每次5 min;训练2组大鼠每天游泳1次,每次10 min;训练3组大鼠每天游泳2次,每次10 min;对照组大鼠不做任何训练;另15只鼠为假手术组不阻塞大脑中动脉血流,不训练.采用Garcia神经功能缺损评分评价神经功能缺损情况.采用TUNEL染色观察缺血区大脑皮质细胞凋亡情况.应用免疫组织化学法对脑缺血后脑内神经生长抑制因子Sema 3A及其受体NP-1的表达进行分析.结果 假手术组神经行为功能正常.对照组各时间点的Garcia神经行为功能评分与假手术组同时间点比较,差异均有统计学意义(P<0.01);各训练组游泳训练7和14 d后的Garcia神经功能评分明显优于同时间点对照组(P<0.01),且训练3组神经功能评分提高最明显,其游泳训练3、7和14 d后的Garcia神经功能评分分别为(12.80±0.45)、(15.20±0.45)和(16.80±0.45)分.游泳训练3、7和14 d后,训练1组、训练2组、训练3组的Sema3A、NP-1及TUNEL各指标阳性细胞的表达均明显低于对照组相同时间点(P<0.01),以训练3组更为明显.训练3组游泳训练3、7和14d后,TUNEL阳性细胞率分别为(29.43±1.38)%、(22.30±1.21)%和(17.58±1.70)%;Sema 3A阳性细胞率分别为(19.64±1.17)%、(9.73±3.83)%和(8.24±0.87)%;NP-1阳性细胞率分别为(33.95±6.86)%、(27.95 ±1.29)%和(18.90±1.44)%,较其他各训练组的阳性细胞表达减少更明显(P<0.01或0.05).结论 康复训练可减少脑缺血再灌注大鼠Sema 3A、NP-1及TUNEL阳性细胞表达,促进其运动功能的恢复及神经功能重塑,强化运动训练的效果更明显.
目的 觀察不同彊度運動訓練對腦缺血再灌註大鼠腦內臂闆蛋白3A(Sema3A)及其受體神經纖毛蛋白-1(NP-1)的錶達以及缺血側腦細胞凋亡的影響,探討彊化運動訓練促進腦缺血再灌註大鼠運動功能恢複的可能機製.方法 採用線栓法建立左側大腦中動脈阻塞( MCAO)2 h再灌註動物模型.60隻造模成功的雄性Wistar大鼠按隨機數字錶法分為訓練1組、訓練2組、訓練3組、對照組(各15隻鼠).訓練1組大鼠每天遊泳1次,每次5 min;訓練2組大鼠每天遊泳1次,每次10 min;訓練3組大鼠每天遊泳2次,每次10 min;對照組大鼠不做任何訓練;另15隻鼠為假手術組不阻塞大腦中動脈血流,不訓練.採用Garcia神經功能缺損評分評價神經功能缺損情況.採用TUNEL染色觀察缺血區大腦皮質細胞凋亡情況.應用免疫組織化學法對腦缺血後腦內神經生長抑製因子Sema 3A及其受體NP-1的錶達進行分析.結果 假手術組神經行為功能正常.對照組各時間點的Garcia神經行為功能評分與假手術組同時間點比較,差異均有統計學意義(P<0.01);各訓練組遊泳訓練7和14 d後的Garcia神經功能評分明顯優于同時間點對照組(P<0.01),且訓練3組神經功能評分提高最明顯,其遊泳訓練3、7和14 d後的Garcia神經功能評分分彆為(12.80±0.45)、(15.20±0.45)和(16.80±0.45)分.遊泳訓練3、7和14 d後,訓練1組、訓練2組、訓練3組的Sema3A、NP-1及TUNEL各指標暘性細胞的錶達均明顯低于對照組相同時間點(P<0.01),以訓練3組更為明顯.訓練3組遊泳訓練3、7和14d後,TUNEL暘性細胞率分彆為(29.43±1.38)%、(22.30±1.21)%和(17.58±1.70)%;Sema 3A暘性細胞率分彆為(19.64±1.17)%、(9.73±3.83)%和(8.24±0.87)%;NP-1暘性細胞率分彆為(33.95±6.86)%、(27.95 ±1.29)%和(18.90±1.44)%,較其他各訓練組的暘性細胞錶達減少更明顯(P<0.01或0.05).結論 康複訓練可減少腦缺血再灌註大鼠Sema 3A、NP-1及TUNEL暘性細胞錶達,促進其運動功能的恢複及神經功能重塑,彊化運動訓練的效果更明顯.
목적 관찰불동강도운동훈련대뇌결혈재관주대서뇌내비판단백3A(Sema3A)급기수체신경섬모단백-1(NP-1)적표체이급결혈측뇌세포조망적영향,탐토강화운동훈련촉진뇌결혈재관주대서운동공능회복적가능궤제.방법 채용선전법건립좌측대뇌중동맥조새( MCAO)2 h재관주동물모형.60지조모성공적웅성Wistar대서안수궤수자표법분위훈련1조、훈련2조、훈련3조、대조조(각15지서).훈련1조대서매천유영1차,매차5 min;훈련2조대서매천유영1차,매차10 min;훈련3조대서매천유영2차,매차10 min;대조조대서불주임하훈련;령15지서위가수술조불조새대뇌중동맥혈류,불훈련.채용Garcia신경공능결손평분평개신경공능결손정황.채용TUNEL염색관찰결혈구대뇌피질세포조망정황.응용면역조직화학법대뇌결혈후뇌내신경생장억제인자Sema 3A급기수체NP-1적표체진행분석.결과 가수술조신경행위공능정상.대조조각시간점적Garcia신경행위공능평분여가수술조동시간점비교,차이균유통계학의의(P<0.01);각훈련조유영훈련7화14 d후적Garcia신경공능평분명현우우동시간점대조조(P<0.01),차훈련3조신경공능평분제고최명현,기유영훈련3、7화14 d후적Garcia신경공능평분분별위(12.80±0.45)、(15.20±0.45)화(16.80±0.45)분.유영훈련3、7화14 d후,훈련1조、훈련2조、훈련3조적Sema3A、NP-1급TUNEL각지표양성세포적표체균명현저우대조조상동시간점(P<0.01),이훈련3조경위명현.훈련3조유영훈련3、7화14d후,TUNEL양성세포솔분별위(29.43±1.38)%、(22.30±1.21)%화(17.58±1.70)%;Sema 3A양성세포솔분별위(19.64±1.17)%、(9.73±3.83)%화(8.24±0.87)%;NP-1양성세포솔분별위(33.95±6.86)%、(27.95 ±1.29)%화(18.90±1.44)%,교기타각훈련조적양성세포표체감소경명현(P<0.01혹0.05).결론 강복훈련가감소뇌결혈재관주대서Sema 3A、NP-1급TUNEL양성세포표체,촉진기운동공능적회복급신경공능중소,강화운동훈련적효과경명현.
Objective To observe the effects of intensive training at different intensities on the expressions of semaphorin 3A ( Sema 3A) and its receptor neuropilin ( NP-1 ) and the cell apoptosis in cerebrum after cerebral ischemia-reperfusion in rats,and to investigate the possible mechanism of intensive training in recovery of motor function after cerebral ischemia-reperfusion in rats. Methods To establish animal model of cerebral ischemia-reperfusion in rats,the intraluminal thread method was applied to cause left middle cerebral artery occlusion (MCAO) for 2 h and before reperfusion.After cerebral ischemia-reperfusion model were established for 24 h,60 male model Wistar rats were randomly divided into training group 1 ( swimming for 5 min once a day),training group 2 ( swimming for 10 min once a day),training group 3 (swimming for 10 min twice a day) and control group (no training) ; another 15 rats assigned to the sham-operation group were subject to no MCAO and no training.Neurological function was evaluated by Garcia scores,and terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) was performed to dectect the cortical cell apoptosis.Expressions of neural growth inhibition factor Sema 3A and its receptor NP-1 were detected by immunohistochemistry. Results The neurological function in sham-operation group was normal.The differences of Garcia scores at different time points beween sham-operation group and control group were significant (P < 0.01 ).Garcia scores in all training groups,were significantly higher than those in controls at the 7th and 14th d after swimming training ( P < 0.01 ),especially in training group 3 the Garcia scores were ( 12.80 ± 0.45 ),( 15.20 ± 0.45 ),( 16.80 ± 0.45 ),respectively,at the 3rd,7th and 14th d after swimming training.The rates of positive cell of Sema 3A,NP-1 and TUNEL indexes in all training groups were lower than those in controls at the 3rd,7th and 14th d after swimming training (P < 0.01 ),especially in the training group 3.At the 3rd,7th and 14th d after swimming training in training group 3,the rates of TUNEL indexes positive apoptosis cells were ( 29.43 ± 1.38 ) %,( 22.30 ± 1.21 ) %,( 17.58 ± 1.70) %,respectively,the positive cell rates of Sema 3A were ( 19.64 ± 1.17) %,(9.73 ± 3.83)%,(8.24 ± 0.87)%,respectively,the positive cell rates of NP-1 were ( 33.95 ± 6.86) %,( 27.95 ± 1.29 ) %,( 18.90 ± 1.44 ) %,respectively,the reduction of positive cells expressions in training group 3 was significantly more obvious compared with other training groups (P < 0.01 or 0.05). Conclusions Rehabilitation training can reduce the expression of positive cell of Sema 3A,NP-1 and TUNEL indexes in rats after cerebral ischemia-reperfusion and can improve motor function recovery and facilitate neural plasticity.The more intensive the training,the better the effects.