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作 者:位庚[1,2] 申瑞霞 李创[1] 张中华[1] 侯凤英 WEI Geng;SHEN Ruixia;LI Chuang;ZHANG Zhonghua;HOU Fengying(The Second Hospital of Shijiazhuang, Hebei 050051, China)
机构地区:[1]石家庄市第二医院,河北050051 [2]络病研究与创新中药国家重点实验室
出 处:《医学动物防制》2018年第6期562-565,569,共5页Journal of Medical Pest Control
基 金:国家重点基础研究发展计划(2012CB518606);石家庄市科学技术研究与发展计划项目(161462343)
摘 要:目的观察同型半胱氨酸(homocysteine,Hcy)对大鼠心肌微血管内皮细胞(rat cardiac microvascular endothelial cells,RCMECs)的炎症损伤及通心络(Tongxinluo,TXL)的干预作用。方法实验分为对照组、模型组和通心络低、中、高剂量组。观察各组细胞的形态;检测生存活性、细胞间粘附因子-1(intercellular adhesion molecule-1,ICAM-1)、白介素-6(interleukin-6,IL-6)、活性氧簇(reactive oxygen species,ROS)及核转录因子-κB(nuclear factor-κB,NF-κB)。结果模型组细胞形态明显受损,细胞生存活性降低,细胞上清液中ICAM-1和IL-6含量升高,细胞内ROS水平升高,NF-κB蛋白表达上调;与模型组相比,通心络中、高剂量组细胞形态明显改善,ICAM-1和IL-6释放减少,细胞内ROS水平降低,NF-κB蛋白表达下调,各组间比较差异有统计学意义(生存活性:F=13.055,P<0.001;ICAM-1:F=11.298,P<0.001;IL-6:F=30.843,P<0.001;ROS:F=3.386,P=0.043;NF-κB:F=77.457,P<0.001)。结论通心络可减轻Hcy对RCMECs的损伤,其作用机制可能与减轻炎症反应有关。Objective To observe the inflammatory injury of homocysteine-induced Rat cardiac microvascular endothelial cells(RCMECs) and the intervention of Tongxinluo(TXL). Methods The experiment included control group,model group,Tongxinluo low dose group,Tongxinluo middle dose group and Tongxinluo high dose group. The morphological changes of the cells were observed,and the cell viability,interleukin-6(IL-6),intercellular adhesion molecule-1(ICAM-1),reactive oxygen species(ROS) in cells,and the levels of nuclear factor-κB(NF-κB) were detected. Results Compared with the control group,cells morphology was significantly impaired,cell viability being significantly decreased. ICAM-1 and IL-6 content of cell supernatant,the production of ROS and the protein expression of NF-κB were significantly increased in model group(P〈0. 01). Compared with the model group,cells morphology was significantly improved,IL-6 and ICAM-1 content of cell supernatant,and ROS production and NF-κB protein expression being significantly decreased in Tongxinluo middle group and Tongxinluo high group,and there was a statistical difference between the groups(cell viability: F = 13. 055,P〈0. 001;ICAM-1: F = 11. 298, P〈0. 001; IL-6: F = 30. 843, P〈0. 001; ROS: F = 3. 386, P = 0. 043; NF-κB: F =77. 457,P〈0. 001). Conclusion TXL could alleviate the damage of RCMECs resulting from Hcy,and its mechanism might be associated with reducing inflammatory response.
关 键 词:通心络 大鼠心肌微血管内皮细胞 同型半胱氨酸 炎症损伤
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