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阿替普酶對急性腦梗死大鼠血管內皮細胞中Claudin-1和Claudin-5蛋白表達的影響

發(fā)布時間:2018-02-28 21:32

  本文關鍵詞: 阿替普酶 急性腦梗死 血管內皮細胞 閉合蛋白 閉合蛋白 出處:《吉林大學學報(醫(yī)學版)》2017年06期  論文類型:期刊論文


【摘要】:目的:探討阿替普酶對急性腦梗死大鼠溶栓后血管內皮細胞中閉合蛋白1(Claudin-1)和閉合蛋白5(Claudin-5)表達的影響及保護作用機制,為阿替普酶的臨床應用提供依據(jù)。方法:建立大鼠急性大腦中動脈栓塞模型。54只SD大鼠隨機分為假手術組、模型組和阿替普酶溶栓組,每組18只。透射電子顯微鏡下觀察大鼠腦內皮細胞超微結構,熒光免疫組織化學法和Western blotting法檢測大鼠血管內皮細胞中Claudin-1和Claudin-5蛋白的表達水平。結果:透射電子顯微鏡檢測,模型組大鼠缺血區(qū)域腦體積明顯增大,內皮細胞腫脹,部分皮質與周圍腦組織界限明顯,基膜厚薄均勻,緊密連接結構非常松散、出現(xiàn)斷裂和消失;阿替普酶溶栓組大鼠腦梗死區(qū)域毛細血管內皮細胞腫脹明顯減輕,基膜厚薄不均勻改善,腦毛細血管內皮細胞、內皮細胞之間大部分緊密連接結構斷裂情況消失,無緊密連接結構消失。熒光免疫組織化學檢測,與模型組比較,阿替普酶溶栓組大鼠血管內皮細胞中Claudin-1和Claudin-5蛋白的表達有明顯改善。Western blotting檢測,與假手術組比較,模型組大鼠血管內皮細胞中Claudin-1和Claudin-5蛋白表達水平明顯減少(P0.01);與模型組比較,不同時間點阿替普酶溶栓組大鼠血管內皮細胞中Claudin-1和Claudin-5蛋白表達水平均升高(P0.01)。結論:阿替普酶對急性腦梗死大鼠大腦內皮細胞的結構有改善作用,其作用機制可能與阿替普酶能降低大鼠血管內皮細胞中Claudin-1和Claudin-5蛋白表達水平有關。
[Abstract]:Objective: to investigate the effect of atropase on the expression of closure protein 1 Claudin-1 and closure protein 5 Claudin-5 in vascular endothelial cells of rats with acute cerebral infarction after thrombolytic therapy and its protective mechanism. Methods: 54 SD rats with acute middle cerebral artery embolization were randomly divided into sham-operation group, model group and atropase thrombolytic group. The ultrastructure of rat brain endothelial cells was observed under transmission electron microscope, and the expression of Claudin-1 and Claudin-5 protein in rat vascular endothelial cells was detected by fluorescence immunohistochemical method and Western blotting method. Results: transmission electron microscopy was used to detect the expression of Claudin-1 and Claudin-5 protein in rat vascular endothelial cells. In the model group, the cerebral volume of ischemic area was obviously enlarged, the endothelial cells were swollen, the boundary between some cortex and peripheral brain tissue was obvious, the thickness of basement membrane was uniform, the tight junction structure was very loose, and the rupture and disappearance occurred. The swelling of capillary endothelial cells in the cerebral infarction area was obviously reduced, the thickness of the basement membrane was improved inhomogeneously, and most of the tight junctions between the cerebral capillary endothelial cells and the endothelial cells disappeared in the AtiP thrombolytic group. Compared with the model group, the expression of Claudin-1 and Claudin-5 protein in the vascular endothelial cells of the rats treated with atropase thrombolytic therapy was significantly improved. Western blotting was detected, and compared with the sham-operated group, the expression of Claudin-1 and Claudin-5 protein in the vascular endothelial cells of the rats treated with atropase thrombolytic therapy was significantly improved. The expression of Claudin-1 and Claudin-5 protein in vascular endothelial cells of the model group was significantly decreased compared with the model group. At different time points, the expression of Claudin-1 and Claudin-5 protein in vascular endothelial cells were increased in rats treated with atropase at different time points. Conclusion: Atiprase can improve the structure of cerebral endothelial cells in rats with acute cerebral infarction. The mechanism may be related to the decrease of Claudin-1 and Claudin-5 protein expression in rat vascular endothelial cells by atropase.
【作者單位】: 承德醫(yī)學院附屬醫(yī)院神經(jīng)內科;
【基金】:河北省科技廳科研項目資助課題(15277752D) 河北省承德市科技局自籌項目資助課題(20157044)
【分類號】:R743.33

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