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作 者:林卫红[1] 马涤辉[1] 崔俐[1] 谢晓娜[2] 姜慧轶[3] 王绍[4]
机构地区:[1]吉林大学第一医院神经内科,吉林长春130021 [2]吉林大学第一医院内分泌科,吉林长春130021 [3]吉林大学第一医院儿科,吉林长春130021 [4]吉林大学基础医学院生理学教研室,吉林长春130021
出 处:《吉林大学学报(医学版)》2008年第3期381-384,F0002,共5页Journal of Jilin University:Medicine Edition
基 金:吉林省科技厅基金资助课题(20050407-6)
摘 要:目的:探讨大鼠脑胶质瘤缝隙连接蛋白在抑胶素干预下的表达变化,阐明抑胶素抑制脑胶质瘤的多源性调节机制。方法:体外培养大鼠C6脑胶质瘤细胞,制作大鼠脑胶质瘤模型,分为空白对照组及不同浓度抑胶素实验组(Ⅰ、Ⅱ、Ⅲ和Ⅳ,8、16、32和64μg.kg-1),各实验组腹腔注射抑胶素,利用免疫组织化学染色法及Western blotting法检测不同浓度抑胶素对大鼠脑胶质瘤缝隙连接蛋白43(CX43)免疫反应阳性细胞数及表达量的影响。结果:对照组及8、16、32和64μg.kg-1抑胶素组大鼠脑胶质瘤CX43免疫反应阳性细胞数分别为(4.31±1.24)、(5.23±2.01)、(11.58±3.21)、(20.13±3.04)和(23.58±4.32)个/视野,各实验组与对照组比较差异均有显著性(P<0.05或P<0.01),各实验组组间两两比较差异均具有显著性(P<0.01);对照组及8、16、32和64μg.kg-1抑胶素组大鼠脑胶质瘤CX43表达量(蛋白条带的面积和平均灰度相乘量)分别为12 241、12 377、16 183、17 138和28 208,各实验组与对照组比较差异均有显著性(P<0.05或P<0.01),各实验组组间两两比较差异均具有显著性(P<0.01)。结论:抑胶素对脑胶质瘤的抑制作用可能与影响肿瘤细胞间的缝隙连接蛋白功能有关。Objective To explore the changes of the expression of connexin 43 in rat glioma treated by antigliomatin and research multi-originated regulatory mechanism of antigliomatin's suppression on glioma. Methods C6 glioma cells were cultivated in vitro, which were used to make model of rat glioma. These cells were divided into control group and experimental groups treated with different concentrations of antigliomatin ( 8, 16, 32 and 64 μg · kg^-1). Antigliomatin was given by peritoneal injection in experimental groups. The effects of antigliomatin with different concentrations on the expression of CX43-immunoreaction positive cells were determined by immunohistochemical staining method and Western blotting. Results The number of CX43-immunoreaction positive cells in control group and 8, 16, 32 and 64 μg·kg^-1 antigliomatin groups were 4.31±1.24, 5.23±2.01, 11.58±3.21, 20.13 ±3.04 and 23.58±4.32 in each visual field, there were significant differences between control group and experimental groups (P〈0.05 or P〈0.01), and there also were significant differences between experimental groups (P〈 0.01). The amounts of CX43-expression (cross product of albumen-strap's area and average gray scale) in control group and 8, 16, 32 and 64 μg · kg^-1 antigliomatin groups were 12241, 12 377, 16 183, 17 138 and 28 208, there were significant differences between control group and experimental groups (P〈0. 05 or P〈0. 01), and there also were significant differences between experimental groups (P 〈 0.01). Conclusion The inhibitory effects of antigliomatin on glioma may be related to influence of connexin function.
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