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糖尿病小鼠局灶性腦缺血再灌注損傷中腦周細胞的變化

發(fā)布時間:2018-01-22 02:32

  本文關鍵詞: 腦缺血再灌注 高血糖 周細胞 α-平滑肌肌動蛋白 出處:《安徽醫(yī)科大學學報》2017年11期  論文類型:期刊論文


【摘要】:目的探討糖尿病高血糖狀態(tài)下局灶腦缺血再灌注損傷中腦周細胞的變化特點。方法采用四氧嘧啶一次性腹腔注射制備1型糖尿病高血糖C57BL/6小鼠模型,以線栓法為基礎使大腦中動脈缺血建立局灶性腦缺血再灌注小鼠模型,使用行為學、組織化學、qRT-PCR及Western blot等方法,對比觀察假手術組(空白對照組)、正常血糖腦缺血再灌注組(缺血組)、糖尿病高血糖腦缺血再灌注組(高糖并缺血組)大腦皮質區(qū)周細胞數(shù)量改變和α-平滑肌肌動蛋白(α-SMA)的相對表達情況。結果免疫組化及TTC染色顯示,與空白對照組比較,缺血組缺血1 h再灌注24 h后腦組織中α-SMA陽性細胞數(shù)量明顯增多,梗死腦組織水腫明顯(P0.05);高糖并缺血組再灌注24 h,α-SMA陽性細胞數(shù)目較同期缺血組更多,梗死區(qū)域水腫極嚴重(P0.05);qRT-PCR和Western blot分別顯示高糖并缺血組α-SMA蛋白對應基因、α-SMA蛋白的相對表達量均高于缺血組(P0.05)。結論糖尿病高血糖與缺血再灌注兩種損傷機制同時作用于腦組織時,使腦組織損傷更嚴重,損傷區(qū)域α-SMA的表達增強,周細胞數(shù)量明顯增加。
[Abstract]:Objective to investigate the changes of pericyte in focal cerebral ischemia-reperfusion injury induced by diabetic hyperglycemia. Methods the model of type 1 diabetes with hyperglycemia C57BL / 6 was established by single intraperitoneal injection of alloxan. . The animal model of focal cerebral ischemia reperfusion was established by middle cerebral artery ischemia on the basis of thread embolization. Behavior, histochemical qRT-PCR and Western blot were used. The sham operation group (blank control group) and the normal blood glucose cerebral ischemia reperfusion group (ischemia group) were observed. Changes in the number of pericortex cells and 偽 -smooth muscle actin (偽 -SMA) in the hyperglycemic cerebral ischemia-reperfusion group (hyperglycemia with ischemia group). Results Immunohistochemistry and TTC staining showed. Compared with the blank control group, the number of 偽 -SMA positive cells in cerebral tissue of ischemic group increased significantly after 1 h of ischemia and 24 h of reperfusion, and the edema of infarcted brain tissue was significantly increased (P 0.05). After 24 h reperfusion, the number of 偽 -SMA positive cells in high glucose with ischemia group was more than that in ischemia group, and the edema in infarct area was very serious (P 0.05). QRT-PCR and Western blot showed 偽 -SMA protein corresponding genes in hyperglycemia and ischemia group respectively. The relative expression of 偽 -SMA protein was higher than that of ischemia group (P 0.05). Conclusion the hyperglycemia and ischemia-reperfusion injury mechanism in the brain tissue at the same time make the brain tissue damage more serious. The expression of 偽 -SMA was increased and the number of pericytes was increased.
【作者單位】: 安徽醫(yī)科大學第二附屬醫(yī)院神經(jīng)外科;安徽醫(yī)科大學藥學院;
【基金】:國家自然科學基金(編號:31540021)
【分類號】:R587.2;R743
【正文快照】: 周細胞是血管神經(jīng)單元的重要組成成分之一,廣泛分布于全身各組織如腦、心臟、眼睛等的微血管和毛細血管壁而被微血管基底膜包被,位于內皮細胞外,其具有多種功能并在腦部參與血腦屏障功能的維持[1-2]。α-平滑肌肌動蛋白(α-smooth muscleactin,α-SMA)是微絲的線性結構蛋白,是

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