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机构地区:[1]中国人民解放军海军总医院干部呼吸科,北京100048
出 处:《郑州大学学报(医学版)》2013年第6期799-802,共4页Journal of Zhengzhou University(Medical Sciences)
基 金:全军医药卫生科研基金资助项目36040
摘 要:目的:观察益肺活血复方对人肺动脉内皮细胞微结构及内分泌功能的影响。方法:建立人肺动脉内皮细胞低氧高二氧化碳模型;制备益肺活血复方不同给药剂量(生药10、20、40 g/kg)的含药血清;在细胞培养液中共同孵育12 h后,利用透射电镜观察细胞微结构变化,采用放射免疫法测定各组细胞培养液上清中内皮素-1(ET-1)及前列环素(PGI2)的含量,采用硝酸还原酶法测定细胞培养液中一氧化氮(NO)的含量。结果:低氧高二氧化碳条件下,人肺动脉内皮细胞微结构损伤,而中、高剂量益肺活血复方组细胞微结构损伤减轻。各组细胞培养液或培养液上清中ET-1、NO、PGI2的含量比较,差异有统计学意义(F=121.870、60.040、49.060,P均<0.001);模型组ET-1含量高于空白对照组,NO、PGI2含量低于空白对照组(P均<0.01);中、高剂量益肺活血复方组ET-1含量低于模型组,NO和PGI2含量高于模型组(P均<0.01)。结论:低氧高二氧化碳导致人肺动脉内皮细胞微结构及功能障碍,而中、高剂量益肺活血复方可减轻其结构及功能损伤的程度。Aim:To investigate the effects of Compound Yifei Huoxue( CYH) on the cell microstructure and secretion function of human pulmonary artery endothelial cells. Methods:A model of hypoxia hypercapnia was established. Different doses of pharmacy( 10,20,40 g / kg crude drug) were added into the culture medium to prepare serum containing CYH.After incubation for 12 h,the cell microstructure was observed by transmission electron microscopy,the levels of ET-1 and PGI2were tested by radioimmunoassay method,and NO level was tested by nitrate reductase. Results:Hypoxic hypercapnia caused damage to the cell microstructure,while moderate and high dose CYH could alleviate the damage. There were significant differences in the levels of ET-1,NO and PGI2among 3 CYH model group and blank control group( F =121. 870,60. 040,49. 060,P 0. 001). The level of ET-1 in the model group was higher than that of blank control group,but the levels of NO and PGI2were lower( P 0. 01). The levels of ET-1 in moderate and high dose CYH groups were lower than that of model group,but the levels of NO and PGI2were higher( P 0. 01). Conclusion:Hypoxia hypercapnia could cause human pulmonary artery endothelial cell microstructure damage and dysfunction. Moderate and high dose CYH could alleviate the damage.
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