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
2011年
10期
736-740
,共5页
黄杰%马玉娟%方征宇%种玉飞%随燕芳%尤春景
黃傑%馬玉娟%方徵宇%種玉飛%隨燕芳%尤春景
황걸%마옥연%방정우%충옥비%수연방%우춘경
脑梗死%高频重复经颅磁刺激%超微结构%脑源性神经营养因子
腦梗死%高頻重複經顱磁刺激%超微結構%腦源性神經營養因子
뇌경사%고빈중복경로자자격%초미결구%뇌원성신경영양인자
Cerebral infarction%High frequency repetitive transcranial magnetic stimulation%Ultrastructure%Brain-derived neurotrophic factor
目的 观察不同强度高频重复经颅磁刺激(rTMS)对脑梗死大鼠缺血半暗带超微结构及脑源性神经营养因子(BDNF)表达的影响.方法 将42只SD大鼠分为正常组、模型组、假刺激组及rTMS组,其中rTMS组按不同刺激强度又细分为80%运动阈值(MT)组、100% MT组及120% MT组.将模型组、假刺激组、rTMS组制成右侧大脑中动脉栓塞模型,rTMS组各亚组大鼠于制模24 h后分别给予不同强度20 Hz rTMS刺激,假刺激组大鼠给予假性磁刺激,模型组于制模后未给予其他特殊处理.于实验进行14 d后采用透射电镜、免疫组化及免疫印迹(WB)技术观察各组大鼠缺血半暗带超微结构及BDNF表达.结果 通过电镜观察发现,rTMS组各亚组大鼠缺血半暗带区超微结构损伤明显轻于模型组及假刺激组;通过WB技术检测发现,100% MT组和正常组BDNF光密度值均较假刺激组明显增高(P<0.05),正常组和rTMS组各亚组BDNF光密度值虽然也高于模型组,但组间差异无统计学意义(P>0.05);通过免疫组化技术检测发现,各组大鼠BDNF阳性光密度值组间差异均无统计学意义(P>0.05).结论 20 Hz、特定强度(尤其是100% MT)rTMS能促进脑梗死大鼠缺血半暗带超微结构修复及BDNF表达,这可能是磁刺激治疗缺血性脑卒中的重要机制之一.
目的 觀察不同彊度高頻重複經顱磁刺激(rTMS)對腦梗死大鼠缺血半暗帶超微結構及腦源性神經營養因子(BDNF)錶達的影響.方法 將42隻SD大鼠分為正常組、模型組、假刺激組及rTMS組,其中rTMS組按不同刺激彊度又細分為80%運動閾值(MT)組、100% MT組及120% MT組.將模型組、假刺激組、rTMS組製成右側大腦中動脈栓塞模型,rTMS組各亞組大鼠于製模24 h後分彆給予不同彊度20 Hz rTMS刺激,假刺激組大鼠給予假性磁刺激,模型組于製模後未給予其他特殊處理.于實驗進行14 d後採用透射電鏡、免疫組化及免疫印跡(WB)技術觀察各組大鼠缺血半暗帶超微結構及BDNF錶達.結果 通過電鏡觀察髮現,rTMS組各亞組大鼠缺血半暗帶區超微結構損傷明顯輕于模型組及假刺激組;通過WB技術檢測髮現,100% MT組和正常組BDNF光密度值均較假刺激組明顯增高(P<0.05),正常組和rTMS組各亞組BDNF光密度值雖然也高于模型組,但組間差異無統計學意義(P>0.05);通過免疫組化技術檢測髮現,各組大鼠BDNF暘性光密度值組間差異均無統計學意義(P>0.05).結論 20 Hz、特定彊度(尤其是100% MT)rTMS能促進腦梗死大鼠缺血半暗帶超微結構脩複及BDNF錶達,這可能是磁刺激治療缺血性腦卒中的重要機製之一.
목적 관찰불동강도고빈중복경로자자격(rTMS)대뇌경사대서결혈반암대초미결구급뇌원성신경영양인자(BDNF)표체적영향.방법 장42지SD대서분위정상조、모형조、가자격조급rTMS조,기중rTMS조안불동자격강도우세분위80%운동역치(MT)조、100% MT조급120% MT조.장모형조、가자격조、rTMS조제성우측대뇌중동맥전새모형,rTMS조각아조대서우제모24 h후분별급여불동강도20 Hz rTMS자격,가자격조대서급여가성자자격,모형조우제모후미급여기타특수처리.우실험진행14 d후채용투사전경、면역조화급면역인적(WB)기술관찰각조대서결혈반암대초미결구급BDNF표체.결과 통과전경관찰발현,rTMS조각아조대서결혈반암대구초미결구손상명현경우모형조급가자격조;통과WB기술검측발현,100% MT조화정상조BDNF광밀도치균교가자격조명현증고(P<0.05),정상조화rTMS조각아조BDNF광밀도치수연야고우모형조,단조간차이무통계학의의(P>0.05);통과면역조화기술검측발현,각조대서BDNF양성광밀도치조간차이균무통계학의의(P>0.05).결론 20 Hz、특정강도(우기시100% MT)rTMS능촉진뇌경사대서결혈반암대초미결구수복급BDNF표체,저가능시자자격치료결혈성뇌졸중적중요궤제지일.
Objective To investigate the effects of high-frequency repetitive transcranial magnetic stimulation (rTMS) at different intensities on the ultrastructure of an ischemic brain penumbra and the expression of brainderived neurotrophic factor (BDNF) using rats with permanent middle cerebral artery occlusion (MCAO).Methods Forty-two rats were randomly divided into a blank control group,an MCAO model control group,a sham stimulation control group and an rTMS group.The rTMS group was divided further into 3 subgroups:an 80% of motor threshold (MT) subgroup,a 100% of MT subgroup and a 120% of MT subgroup.The cerebral infarction model was established by right MCAO.rTMS treatment was given 24 hours after the MCAO model was successfully established.The rTMS group and sham stimulation control group were given 20 Hz rTMS with the planned intensities.The MCAO model control group was not given any stimulation.After 14 days of treatment,transmission electron microscopy,immunohistochemical and Western blotting ( WB ) methods were used to investigate the ultrastructure of the ischemic penumbra and the expression of BDNF.Results Damage reflected in the ultrastructure in the 3 rTMS subgroups was less than in the model control group and the sham stimulation control group.Expression of BDNF protein increased significantly in 100% of the MT group and blank control group rats as compared with that in the sham stimulation control group,while the blank control group and the 3 rTMS subgroups had no statistically significant difference in comparison with the MCAO model control group.The expression of BDNF protein had no statistically significant difference between any of the groups.Conclusion 20 Hz rTMS might,especially at 100% of the MT,promote the recovery of the ultrastructure of neural tissues in the ischemic penumbra after acute cerebral infarction and enhance the expression of BDNF in the ipsilesional hemisphere.This may be one of the important mechanisms of rTMS's effectiveness in the treatment of ischemic stroke.