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強(qiáng)制性運(yùn)動(dòng)療法聯(lián)合白脈散有效成分組治療腦卒中運(yùn)動(dòng)功能障礙的研究

發(fā)布時(shí)間:2018-06-02 19:28

  本文選題:強(qiáng)制性運(yùn)動(dòng)療法 + 白脈散有效成分組; 參考:《蘇州大學(xué)》2012年碩士論文


【摘要】:研究目的:研究強(qiáng)制性運(yùn)動(dòng)療法(CIMT)和白脈散有效成分組(ECG)對(duì)腦損傷運(yùn)動(dòng)功能障礙的影響,闡明可能的作用機(jī)制,為相應(yīng)的臨床研究提供理論和實(shí)驗(yàn)依據(jù)。 研究方法:本實(shí)驗(yàn)以二月齡雄性SD大鼠為實(shí)驗(yàn)對(duì)象,線栓法制備大腦中動(dòng)脈栓塞(MCAO/R)致中樞神經(jīng)性運(yùn)動(dòng)功能障礙模型,合格大鼠分為6組(每組10只):模型組(MCAO/R,靜注溶媒)、陽(yáng)性對(duì)照組(MCAO/R,靜注銀杏葉提取物EGB)、強(qiáng)制性運(yùn)動(dòng)療法組(MCAO/R,運(yùn)動(dòng)療法,CIMT組)、ECG組(MCAO/R,靜注ECG)、聯(lián)合治療組(MCAO/R,運(yùn)動(dòng)和靜注ECG組)、假手術(shù)組(Sham,靜注溶媒)。造模后分組干預(yù):CIMT組(15min/次,1次/d×7d),ECG組(150mg.kg-1.d-1,1次/d×7d),EGB組(5.6mg.kg-1.d-1,1次/d×7d)。第7d干預(yù)結(jié)束后即刻全部處死。測(cè)試下列指標(biāo):腦缺血灶組織病理形態(tài)學(xué)結(jié)構(gòu)觀察(HE染色)、細(xì)胞凋亡數(shù)量(TUNEL染色)、試劑盒檢測(cè)自由基相關(guān)指標(biāo)(SOD活性、MDA含量、GSH含量、NOS活性)、免疫組化觀察腦缺血灶皮層凋亡相關(guān)蛋白(Caspase-3及Bcl-2蛋白)表達(dá),體重(測(cè)定時(shí)間:干預(yù)前、干預(yù)后3d、7d)、神經(jīng)行為學(xué)評(píng)分(Long5級(jí)4分法;評(píng)估時(shí)間:干預(yù)前、實(shí)驗(yàn)結(jié)束即刻)。實(shí)驗(yàn)結(jié)果采用SPSS l8.0統(tǒng)計(jì)軟件進(jìn)行分析。 研究結(jié)果:7d干預(yù)結(jié)束后四個(gè)干預(yù)組各指標(biāo)較MCAO/R組均有顯著改善:1、四個(gè)干預(yù)組的體重均有所恢復(fù)。2、四個(gè)干預(yù)組的神經(jīng)行為學(xué)評(píng)分、腦組織病理形態(tài)學(xué)損傷、缺血灶皮層細(xì)胞凋亡數(shù)量均顯著改善,改善程度從高到低依次為:CIMT+ECG組 CIMT組 ECG組≈EGB組。3、四個(gè)干預(yù)組的腦組織中SOD活性、GSH含量、SOD/MDA比值均顯著增高,而MDA含量、NO含量顯著降低,各干預(yù)組抗自由基能力從高到低依次為:CIMT+ECG組 EGB組CIMT組≈ECG組。4、四個(gè)干預(yù)組的腦缺血皮層區(qū)細(xì)胞中Bcl-2蛋白表達(dá)均顯著增高,從高到低依次為:CIMT+ECG組 CIMT組 ECG組≈EGB組;Caspase-3蛋白表達(dá)均顯著減少,從低到高依次為:CIMT+ECG組CIMT組ECG組≈EGB組。 研究結(jié)論:1、本研究制備的腦缺血再灌注模型是有效的。2、CIMT和/或靜注ECG、EGB可以促進(jìn)腦損傷運(yùn)動(dòng)障礙的康復(fù),發(fā)現(xiàn)以上療法可以提高大腦皮層的抗氧化物質(zhì)含量和抗氧化能力,減少腦皮層梗死體積,減少凋亡相關(guān)蛋白含量,減少細(xì)胞凋亡和丟失,促進(jìn)了運(yùn)動(dòng)功能的恢復(fù)。3、CIMT與BMECG對(duì)腦損傷運(yùn)動(dòng)功能障礙大鼠的保護(hù)效果具有相同作用,前者效果好于后者,且均好于EGB(金標(biāo)準(zhǔn)),兩者聯(lián)用效果更佳,,說(shuō)明實(shí)驗(yàn)采取的干預(yù)措施是有效的。
[Abstract]:Objective: to study the effect of compulsory exercise therapy (CIMT) and Baimaisan active component group (ECG) on motor dysfunction of brain injury, to clarify the possible mechanism of action and to provide theoretical and experimental basis for clinical study. Methods: in this study, the male SD rats of two months of age were used to establish the model of central nervous system motor dysfunction induced by middle cerebral artery embolization (MCAO / R). The eligible rats were divided into 6 groups (10 rats in each group): model group (MCAO / R, intravenous injection of solute), positive control group (MCAO / R), intravenous injection of Ginkgo biloba extract (EGBN), mandatory exercise therapy group (MCAO / R), exercise therapy / CIMT group / ECG group, intravenous injection of ECG / R, combined treatment group (MCAO / R), exercise and intravenous injection (MCAO / R). ECG group, sham group, intravenous injection of solute. After the model was established, the rats were divided into two groups: the control group (15 min / d 脳 7 d) and the ECG group (n = 150 mg 路kg ~ (-1) 路d ~ (-1) 路d ~ (-1) / d ~ (-1) 路L ~ (-1) 路d ~ (-1) 路d ~ (-1)? All rats were killed immediately after 7 days of intervention. The following indexes were tested: histopathologic structure of cerebral ischemia focus was observed by HE staining, apoptosis was detected by Tunel staining, SOD activity, MDA content, GSH content and NOS activity were detected by kit, and cerebral ischemia was observed by immunohistochemistry. Expression of Caspase-3 and Bcl-2 protein in focal cortex. Body weight (measurement time: before intervention, 3 days after intervention, 7 days after intervention, neurobehavioral score and Long5 grade 4; evaluation time: before intervention, immediately after intervention. The experimental results were analyzed by SPSS l 8.0 software. Results after 7 days of intervention, each index of the four intervention groups was significantly improved than that of the MCAO/R group. The body weight of the four intervention groups recovered to 0.2. The neurobehavioral score and the pathomorphological injury of brain tissue in the four intervention groups were observed. The number of apoptotic cells in ischemic cortex was significantly improved, the degree of improvement from high to low was as follows: CIMT group, CIMT group, 鈮

本文編號(hào):1969918

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