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
9期
657-661
,共5页
梁慧英%林阳阳%燕铁斌%廖琳%董军涛
樑慧英%林暘暘%燕鐵斌%廖琳%董軍濤
량혜영%림양양%연철빈%료림%동군도
电针%痴呆,血管性%记忆%海马%基因表达
電針%癡呆,血管性%記憶%海馬%基因錶達
전침%치태,혈관성%기억%해마%기인표체
Electroacupuncture%Dementia,vascular%Memory%Hippocampus%Gene expression
目的 观察电针对血管性痴呆(VD)大鼠海马组织GluA1与钙离子/钙调素依赖性蛋白激酶Ⅱ(CaMKⅡ)蛋白表达及磷酸化的影响,探讨电针的治疗作用机制.方法 将Wistar大鼠随机分为假手术组、模型组、模拟针刺组和电针组,每组8只.假手术组暴露双侧颈总动脉,但不结扎;模型组、模拟针刺组和电针组采用双侧颈总动脉永久性结扎法建立VD大鼠模型,以新事物识别实验筛选造模成功大鼠.4组大鼠均采用柔软型大鼠固定器固定.电针组选取百会、足三里穴,接通电流,每日1次,每次留针30 min,连续治疗7d;模拟针刺组在百会、足三里穴以毫针刺入皮下0.5 mm;模型组与假手术组只给予固定,不做其它处理.治疗结束后,采用Western Blot法检测大鼠海马组织GluA1、磷酸化GluA1(pGluA1)、CaMKⅡ、磷酸化的CaMKⅡ(pCaMKⅡ)的表达情况,采用Image J图像分析系统对蛋白表达水平进行分析.结果 模型组、模拟电针组、电针组三组大鼠造模后的探索指数[(0.526±0.112)、(0.541 ±0.124)和(0.498±0.099)]均较假手术组(0.785±0.097)明显降低(P＜0.05);而模型组、模拟针刺组、电针组三组之间两两比较,差异无统计学意义(P＞0.05).模型组大鼠海马组织GluA1、pGluA1、CaMKⅡ和pCaMKⅡ的表达水平[(1.216 ±0.102)、(1.502 ±0.419)、(1.516±0.392)和(0.394±0.227)]均较假手术组[(1.918±0.137)、(2.253±0.244)、(2.187±0.231)、(0.667±0.175)]明显降低(P＜0.05).电针组GluA1、pGluA1、CaMKⅡ和pCaMKⅡ的蛋白表达水平[(1.653±0.169)、(2.382±0.308)、(2.733±0.387)、(1.189±0.346)]明显高于模型组和模拟针刺组[(1.231±0.188)、(1.498±0.223)、(1.493±0.205)和(0.408±0.231)],且组间差异均有统计学意义(P＜0.05).结论 电针可增加VD大鼠海马GluA1及CaMKⅡ的蛋白表达,并促使其发生磷酸化;电针大鼠百会和足三里穴易化LTP和改善VD大鼠学习记忆能力的机制可能是通过诱导沉默突触转化为功能性突触实现的.
目的 觀察電針對血管性癡呆(VD)大鼠海馬組織GluA1與鈣離子/鈣調素依賴性蛋白激酶Ⅱ(CaMKⅡ)蛋白錶達及燐痠化的影響,探討電針的治療作用機製.方法 將Wistar大鼠隨機分為假手術組、模型組、模擬針刺組和電針組,每組8隻.假手術組暴露雙側頸總動脈,但不結扎;模型組、模擬針刺組和電針組採用雙側頸總動脈永久性結扎法建立VD大鼠模型,以新事物識彆實驗篩選造模成功大鼠.4組大鼠均採用柔軟型大鼠固定器固定.電針組選取百會、足三裏穴,接通電流,每日1次,每次留針30 min,連續治療7d;模擬針刺組在百會、足三裏穴以毫針刺入皮下0.5 mm;模型組與假手術組隻給予固定,不做其它處理.治療結束後,採用Western Blot法檢測大鼠海馬組織GluA1、燐痠化GluA1(pGluA1)、CaMKⅡ、燐痠化的CaMKⅡ(pCaMKⅡ)的錶達情況,採用Image J圖像分析繫統對蛋白錶達水平進行分析.結果 模型組、模擬電針組、電針組三組大鼠造模後的探索指數[(0.526±0.112)、(0.541 ±0.124)和(0.498±0.099)]均較假手術組(0.785±0.097)明顯降低(P＜0.05);而模型組、模擬針刺組、電針組三組之間兩兩比較,差異無統計學意義(P＞0.05).模型組大鼠海馬組織GluA1、pGluA1、CaMKⅡ和pCaMKⅡ的錶達水平[(1.216 ±0.102)、(1.502 ±0.419)、(1.516±0.392)和(0.394±0.227)]均較假手術組[(1.918±0.137)、(2.253±0.244)、(2.187±0.231)、(0.667±0.175)]明顯降低(P＜0.05).電針組GluA1、pGluA1、CaMKⅡ和pCaMKⅡ的蛋白錶達水平[(1.653±0.169)、(2.382±0.308)、(2.733±0.387)、(1.189±0.346)]明顯高于模型組和模擬針刺組[(1.231±0.188)、(1.498±0.223)、(1.493±0.205)和(0.408±0.231)],且組間差異均有統計學意義(P＜0.05).結論 電針可增加VD大鼠海馬GluA1及CaMKⅡ的蛋白錶達,併促使其髮生燐痠化;電針大鼠百會和足三裏穴易化LTP和改善VD大鼠學習記憶能力的機製可能是通過誘導沉默突觸轉化為功能性突觸實現的.
목적 관찰전침대혈관성치태(VD)대서해마조직GluA1여개리자/개조소의뢰성단백격매Ⅱ(CaMKⅡ)단백표체급린산화적영향,탐토전침적치료작용궤제.방법 장Wistar대서수궤분위가수술조、모형조、모의침자조화전침조,매조8지.가수술조폭로쌍측경총동맥,단불결찰;모형조、모의침자조화전침조채용쌍측경총동맥영구성결찰법건립VD대서모형,이신사물식별실험사선조모성공대서.4조대서균채용유연형대서고정기고정.전침조선취백회、족삼리혈,접통전류,매일1차,매차류침30 min,련속치료7d;모의침자조재백회、족삼리혈이호침자입피하0.5 mm;모형조여가수술조지급여고정,불주기타처리.치료결속후,채용Western Blot법검측대서해마조직GluA1、린산화GluA1(pGluA1)、CaMKⅡ、린산화적CaMKⅡ(pCaMKⅡ)적표체정황,채용Image J도상분석계통대단백표체수평진행분석.결과 모형조、모의전침조、전침조삼조대서조모후적탐색지수[(0.526±0.112)、(0.541 ±0.124)화(0.498±0.099)]균교가수술조(0.785±0.097)명현강저(P＜0.05);이모형조、모의침자조、전침조삼조지간량량비교,차이무통계학의의(P＞0.05).모형조대서해마조직GluA1、pGluA1、CaMKⅡ화pCaMKⅡ적표체수평[(1.216 ±0.102)、(1.502 ±0.419)、(1.516±0.392)화(0.394±0.227)]균교가수술조[(1.918±0.137)、(2.253±0.244)、(2.187±0.231)、(0.667±0.175)]명현강저(P＜0.05).전침조GluA1、pGluA1、CaMKⅡ화pCaMKⅡ적단백표체수평[(1.653±0.169)、(2.382±0.308)、(2.733±0.387)、(1.189±0.346)]명현고우모형조화모의침자조[(1.231±0.188)、(1.498±0.223)、(1.493±0.205)화(0.408±0.231)],차조간차이균유통계학의의(P＜0.05).결론 전침가증가VD대서해마GluA1급CaMKⅡ적단백표체,병촉사기발생린산화;전침대서백회화족삼리혈역화LTP화개선VD대서학습기억능력적궤제가능시통과유도침묵돌촉전화위공능성돌촉실현적.
Objective To observe the effect of electroacupuncture(EA) on the hippocampal expression of GluA1,pGluA1,CaMK Ⅱ and pCaMK Ⅱ in rats with vascular dementia(VD),so as to find out the underlying mo lecular mechanisms of EA in treating VD.Methods Thirty-two Wistar rats were randomly divided into a shamoperation group,a model group,a sham-acupuncture group,and an EA group (8 in each group).Permanent bilateral common carotid artery occlusion was performed to model vascular dementia in the model group,the shamacupuncture group and the EA group,while exposure but no occlusion of the bilateral common carotid were performed in the sham-operating group.Novel object recognition test was adopted to prove the establishment of VD rat model.All the rats were kept in an immobilization apparatus while receiving treatments.EA was applied onto " Baihui" (GV20) and "Zusanli" (ST36) in EA group for 30 min,once daily for 7 days.Sham-acupuncture group were treated with needles inserted 0.5 mm superficially.And the sham-operation group and the model group were only immobilized.The protein expression of GluA1,pGluA1,CaMK Ⅱ and pCaMK Ⅱ in hippocampal tissue was detected by western blotting.Results The expression of GluA1 in the model group (1.216 ± 0.102) was significantly less than in the sham-operating group (1.918 ± 0.137) (P ＜ 0.05).The expression of GluA1 in the EA group (1.653 ± 0.169) was significantly higher than in the model group (1.216 ± 0.102) and in sham-acupuncture group (1.231 ±0.188) (P＜0.05).The expression of CaMKⅡ in the model group (1.516±0.392) was less than in the sham-operating group (2.187 ± 0.231) (P ＜ 0.05).The expression of CaMK Ⅱ in the EA group (2.733 ±0.387) was significantly higher than in the model group (1.516 ±0.392) and sham-acupuncture group (1.493 ±0.205) (P＜0.05).The expression ofpGluA1 in the model group (1.502 ±0.419) was less than in the sham-operating group (2.253 ± 0.244) (P ＜ 0.05).The expression of pGluA1 in the EA group (2.382 ± 0.308) was significantly higher than in the model group (1.502 ± 0.419) and the sham-acupuncture group (1.498 ± 0.223) (P ＜ 0.05).The expression of pCaMK Ⅱ in the model group (0.394 ± 0.227) was less than in the sham-operating group (0.667 ±0.175) (P＜0.05).The expression ofpCaMKⅡ in the EA group (1.189± 0.346) was significantly higher than in the model group (0.394 ± 0.227) and the sham-acupuncture group (0.408 ± 0.231) (P ＜ 0.05).Conclusion EA can enhance the protein expression and phosporylation of GluA1 and CaMK Ⅱ,causing silent synapses transforming into functional synapses,and consequently,long term potentiation was facilitated and cognitive impairment was improved by EA.
