【摘要】：目的：本研究采用Longa線栓法建立大鼠腦缺血再灌注模型,觀察比較亞低溫治療組與常溫組大鼠神經(jīng)功能缺損評(píng)分、腦梗死體積及海馬區(qū)nestin、caspase-3陽性細(xì)胞表達(dá)情況,目的是探索腦缺血后亞低溫治療的神經(jīng)保護(hù)作用、亞低溫治療對(duì)神經(jīng)再生與細(xì)胞凋亡的影響及可能機(jī)制,為臨床缺血性腦血管病的亞低溫治療提供理論依據(jù)。 方法：將144只SD大鼠隨機(jī)分為三組：假手術(shù)組、缺血再灌注+常溫組、缺血再灌注+亞低溫組。常溫組、低溫治療組據(jù)缺血后再灌注時(shí)間不同各分為1天、3天、7天、14天四個(gè)亞組。采用Longa線栓法建立大鼠腦缺血再灌注模型,亞低溫組于腦缺血模型完成后即刻予4h的全身亞低溫治療,亞低溫治療期間維持大鼠直腸溫度在33-35℃之間,常溫組及假手術(shù)組大鼠直腸溫度維持在36.8～37.2℃之間。Longa評(píng)分法評(píng)估造模前、缺血再灌注各時(shí)間點(diǎn)大鼠的神經(jīng)功能缺損程度,TTC染色法測(cè)量腦梗死體積,免疫組化法檢測(cè)海馬區(qū)nestin陽性細(xì)胞及caspase-3陽性細(xì)胞表達(dá)的情況。 結(jié)果： 1.神經(jīng)功能缺損評(píng)分：假手術(shù)組、常溫組、低溫組三組大鼠術(shù)前Longa評(píng)分均為0分,無統(tǒng)計(jì)學(xué)差異。術(shù)后假手術(shù)組大鼠無神經(jīng)功能缺損癥狀。常溫組、低溫組大鼠再灌注后1天、3天、7天、14天四個(gè)時(shí)間點(diǎn)神經(jīng)功能評(píng)分?jǐn)?shù)值呈逐漸降低趨勢(shì)。再灌注后1天低溫組大鼠神經(jīng)功能缺損評(píng)分與常溫組比較無顯著差異(P0.05),其他三個(gè)時(shí)間點(diǎn)低溫組的神經(jīng)功能評(píng)分均較常溫組降低(P0.05)。 2.大鼠腦梗死體積比較：假手術(shù)組術(shù)后無梗死。常溫組、低溫組均表現(xiàn)為再灌注后1天梗死體積開始增加,再灌注后3天梗死最明顯,隨后逐漸下降。再灌注后1天、3天、7天、14天低溫組大鼠腦梗死體積與常溫組比較均明顯減小(P0.05)。 3.海馬nestin陽性細(xì)胞表達(dá)：假手術(shù)組大鼠海馬可見少量nestin陽性細(xì)胞表達(dá)。常溫組、低溫組海馬nestin陽性細(xì)胞數(shù)隨著再灌注時(shí)間的延長(zhǎng)呈逐漸增加趨勢(shì),再灌注后3天、7天陽性細(xì)胞表達(dá)處于較高水平。再灌注后1天、3天低溫組nestin陽性細(xì)胞數(shù)目均較常溫組增多(P0.05),但再灌注后7天、14天低溫組與常溫組比較陽性細(xì)胞表達(dá)無明顯差異(P0.05)。 4.海馬caspase-3陽性細(xì)胞表達(dá)：假手術(shù)組可見少量陽性細(xì)胞表達(dá)。常溫組、低溫組再灌注后1天時(shí)caspase-3陽性細(xì)胞表達(dá)均處于較高水平,再灌注后3天開始陽性細(xì)胞表達(dá)逐漸下降。再灌注后1天、3天、7天低溫組陽性細(xì)胞數(shù)目均較常溫組降低(P0.05),但再灌注后14天兩組陽性細(xì)胞數(shù)目比較無明顯差異(P0.05)。 結(jié)論： 1.亞低溫(33-35℃)治療能夠改善SD大鼠腦缺血再灌注后神經(jīng)功能缺損癥狀、降低腦梗死體積、促進(jìn)海馬區(qū)nestin陽性細(xì)胞的表達(dá)及抑制caspase-3陽性細(xì)胞的表達(dá)。 2.亞低溫(33～35℃)治療SD大鼠腦缺血再灌注損傷,具有良好的神經(jīng)保護(hù)作用,這可能與亞低溫治療促進(jìn)海馬區(qū)nestin陽性細(xì)胞表達(dá)、抑制caspase-3陽性細(xì)胞表達(dá)有關(guān)。
[Abstract]:Objective: to establish a rat model of cerebral ischemia-reperfusion by Longa thread embolization, and to observe and compare the neurological deficit score, cerebral infarct volume and the expression of nestin,caspase-3 positive cells in hippocampus between mild hypothermia group and normothermic group. Objective to explore the neuroprotective effect of mild hypothermia therapy after cerebral ischemia, the effect of mild hypothermia therapy on nerve regeneration and apoptosis and its possible mechanism, and to provide theoretical basis for mild hypothermia therapy of clinical ischemic cerebrovascular disease. Methods: 144 SD rats were randomly divided into three groups: sham operation group, ischemia reperfusion normal temperature group, ischemia reperfusion mild hypothermia group. The normal temperature group and hypothermia group were divided into four subgroups according to the time of reperfusion after ischemia: 1 day, 3 days, 7 days and 14 days. The rat model of cerebral ischemia reperfusion was established by Longa thread embolization. The mild hypothermia group was treated with mild hypothermia for 4 hours immediately after the completion of cerebral ischemia model, and the rectal temperature was maintained between 33 鈩，

本文編號(hào)：2366920