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大鼠脑出血急性期给予水蛭素后血肿周围组织胶质纤维酸性蛋白的表达
引用本文:吴瑛,任安乐.大鼠脑出血急性期给予水蛭素后血肿周围组织胶质纤维酸性蛋白的表达[J].兰州医学院学报,2009,35(1):1-4.
作者姓名:吴瑛  任安乐
作者单位:吴瑛,WU Ying(兰州大学第一医院康复科,甘肃,兰州730000);任安乐,REN An-le(兰州大学,基础医学院,甘肃,兰州,730000)  
摘    要:目的通过观察水蛭素对大鼠脑出血后血肿周围组织胶质纤维酸性蛋白(GFAP)表达的影响,探讨能否早期应用活血化瘀药物。方法采用胶原酶生理盐水0.8μL(1μL含胶原酶0.5U和肝素6U)注入法制作实验性脑出血动物模型。Wistar大鼠随机分为甘露醇6h、甘露醇3d、水蛭素6h、水蛭素3d、甘露醇+水蛭素6h、甘露醇+水蛭素3d组。光镜下定性观察脑出血后血肿周围脑组织的病理变化;免疫组化染色法观察脑出血后GFAP的表达。结果甘露醇+水蛭素6h组及3d组的灰度值分别高于单用水蛭素组或单用甘露醇组(P〈0.05),且6h组灰度值高于3d组(P〈0.05),说明近期效果优于远期效果。结论脑出血早期在控制脑水肿基础上加用水蛭素可阻止过度的GFAP上调,抑制过度的反应性胶质化,促使星形胶质细胞形态向正常方向发展,可减轻急性期脑组织损伤,脑出血后早期应用水蛭素有可能缩短病程,改善预后。

关 键 词:脑出血  水蛭素  胶质纤维酸性蛋白  免疫组化

Effects of hirudin on the expression of glial fibrillary acidic protein in the surrounding tissues of hematoma at the acute stage of rat apoplexy
WU Ying,REN An-le.Effects of hirudin on the expression of glial fibrillary acidic protein in the surrounding tissues of hematoma at the acute stage of rat apoplexy[J].Journal of Lanzhou Medical College,2009,35(1):1-4.
Authors:WU Ying  REN An-le
Institution:Wu Ying, REN An-le (1. Department of Medical Rehabilitation, First Hospital of Lanzhou University, Lanzhou 730000, China; 2. School of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, China)
Abstract:Objective To investigate the effects of hirudin on the expression of glial fibrillary acidic protein (GFAP) in the surrounding tissues of hematoma at the acute stage of rat apoplexy. Methods Experimental apoplexy animal models was established by injecting 0.8 μL normal saline containing 0.5 U collagenase and 6 U heparin in 1μL of it to Wistar rats, and the rats were randomly divided into 6 h mannitol-treated group, 3 d mannitol-treated group, 6 h hirudin-treated group, 3 d hirudin-treated group, 6 h mannitol plus hirudin-treated group and 3 d mannitol plus hirudin-treated group. The pathological changes in the surrounding tissues of hematoma were observed under light microscope, and expression of GFAP was detected by immunohistochemistry. Results The gray scale was higher in 6 h and 3 d mannitol plus hirudin-treated groups than in 6 h and 3 d mannitol-treated groups and 6 h and 3 d hirudin-treated groups (P 〈0.05), and the gray scale of 6 h groups was higher than that of 3 d groups (P 〈0.05). Conclusion Hirudin may inhibit the upregulation of GFAP expression and excessive reactiveness gumming, spur the development of astrocytes to normal directions and extenuate brain tissue damage at acute stage when given under the control of brain edema at the acute stage of rat apoplexy. Earlier administration of hirudin may also shorten the course of the disease and improve its prognosis after apoplexy.
Keywords:apoplexy  hirudin  glial fibrillary acidic protein  immunohistochemistry
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