节点文献

蒺藜总皂苷对缺氧复氧心肌细胞TNF-α,IL-1β及ICAM-1表达的影响

Effect of gross saponins from Tribulus terrestris L on inflammatory molecules TNF-α,IL-1β and ICAM-1 in cardiocytes with hypoxia/reoxygenation injury

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 殷惠军王显刚史大卓

【Author】 YIN Hui-jun~1 WANG Xian-gang~2 SHI Da-zhuo~1 (1 Xiyuan Hospital,China Academy of Chinese Medical Sciences,Beijing 100091,China;2 Shandong University of Traditional Chinese Medicine,Jinan 250014,China)

【机构】 中国中医科学院西苑医院心内科山东中医药大学中国中医科学院西苑医院心内科 北京 100091济南 250014北京 100091

【摘要】 目的:观察蒺藜总皂苷(gross saponins from Tribulus terrestris L,GSTT)对缺氧复氧心肌细胞炎症分子肿瘤坏死因子-α(TNF-α),白介素1β(IL-1β)及细胞间黏附分子-1(ICAM-1)表达的影响。方法:利用原代培养的SD乳鼠心肌细胞建立心肌缺氧复氧模型,分为正常组、模型组和GSTT高、低浓度(50,10mg·L-1)组。用放免法检测TNF-α和IL-1β,细胞ELISA检测ICAM-1表达。结果:与模型组比较,GSTT高、低浓度(50,10mg·L-1)组TNF-α和IL-1β含量显著降低(P<0.01或P<0.05);GSTT 50 mg·L-1组ICAM-1蛋白表达量显著降低(P<0.05)。结论:GSTT对缺氧复氧损伤心肌细胞有保护作用,其机制与抑制炎性因子TNF-α和IL-1β释放,降低ICAM-1蛋白表达有关。

【Abstract】 Objective:To investigate the effects of gross saponins from Tribulus terrestris L (GSTT) on expression of inflammatory molecules of TNF-α,IL-1βand ICAM-1 in cardiocytes with hy- poxia/regeneration injury.Methods:A model of cardiocytic hypoxia/reoxygenation was induced by pri- mary cultures of cardiocytes of SD neonatal rats in vivo.Subsequently,the cardiocytes were incubated with the GSTT 0,10 or 50 mg·L-1,respectively.Additional healthy eardiocytes of SD rats were used as normal control.TNF-αand IL-1βconcentrations were measured by radioimmunoassay,and ICAM-1 were detected by ELISA.Results:The GSTT (10 and 50 mg·L-1) led to significant reductions of TNF-αand IL-1βlevels (P<0.01,P<0.05).The ICAM-1 levels were significantly decreased in the incubation of the cardioeytes with the GSTT 50 mg·L-1 (P<0.05).Conclusion:The GSTT protected the eardiocytes from hypoxia/regeneratiou injury by inhibiting the release of TNF-αand IL-1βas well as decreasing the expression of ICAM-1.

  • 【文献出处】 中国新药杂志 ,Chinese Journal of New Drugs , 编辑部邮箱 ,2006年22期
  • 【分类号】R285.5
  • 【被引频次】5
  • 【下载频次】199
节点文献中: 

本文链接的文献网络图示:

本文的引文网络