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脂多糖激活补体诱导内皮细胞释放黏附分子和凋亡
引用本文:沈良贤,李敏,孙黔云,石京山.脂多糖激活补体诱导内皮细胞释放黏附分子和凋亡[J].中国药理学通报,2011,27(9):1245-1249.
作者姓名:沈良贤  李敏  孙黔云  石京山
作者单位:1. 贵州省中国科学院天然产物化学重点实验室,贵州,贵阳,550002;遵义医学院,贵州,遵义,563000
2. 贵州省人民医院呼吸疾病研究所,贵州,贵阳,550002
3. 贵州省中国科学院天然产物化学重点实验室,贵州,贵阳,550002
4. 遵义医学院,贵州,遵义,563000
基金项目:国家自然科学基金资助项目,国家重点基础研究发展计划(973计划)资助项目,贵州省优秀科技教育人才省长专项资金资助项目,贵州省优秀青年科技人才项目
摘    要:目的在细胞水平上研究脂多糖(lipopolysaccharide,LPS)激活血清补体对内皮细胞的作用和影响。方法研究LPS激活血清补体的作用方式和特点,观察LPS激活补体对内皮细胞表达黏附分子和凋亡的影响。采用ELISA检测内皮细胞释放P-selectin、E-selectin和ICAM-1的变化,化学发光法检测Caspase-3/7活化情况,SRB法检测LPS激活补体对内皮细胞生长的影响。结果 LPS能够激活血清补体,这种激活呈现量效、时效性。LPS激活血清补体可诱导内皮细胞瞬时明显释放P-selectin,E-selectin和ICAM-1表达也明显上调,同时可导致Caspase-3/7活化。在本实验条件下,LPS激活血清补体对内皮细胞生长未产生抑制。结论 LPS激活血清补体可损伤内皮细胞,导致内皮细胞明显表达黏附分子以及发生凋亡。

关 键 词:脂多糖  补体  内皮细胞  黏附分子  凋亡  补体激活  眼镜蛇毒因子

Adhesion molecule release and apoptosis of endothelial cell induced by lipopolysaccharide-activated complement
SHEN Liang-xian,LI Min,SUN Qian-yun,SHI Jing-shan.Adhesion molecule release and apoptosis of endothelial cell induced by lipopolysaccharide-activated complement[J].Chinese Pharmacological Bulletin,2011,27(9):1245-1249.
Authors:SHEN Liang-xian  LI Min  SUN Qian-yun  SHI Jing-shan
Institution:SHEN Liang-xian1,2,LI Min3,SUN Qian-yun1,SHI Jing-shan2(1.The Key Laboratory of Chemistry for Natural Products,Guizhou Province and Chinese Academy of Sciences,Guiyang 550002,China,2.Zunyi Medical College,Zunyi Guizhou 563000,3.Institute of Respiratory Diseases,Guizhou Provincial People's Hospital,China)
Abstract:Aim To investigate the effects of lipopolysaccharide-activated complement on endothelial cells.Methods The manner of LPS activating complement was characterized.Then the effects of LPS-activated complement on endothelial cells were observed.P-selectin,E-selectin,and ICAM-1 were determined by ELISA.The activity of Caspase-3/7 was measured by chemiluminescence method.The growth of endothelial cells was measured by SRB method.Results LPS activated complement in a dose-and time-dependent manner.The incubation m...
Keywords:lipopolysaccharide  complement  endothelial cell  adhesion molecule  apoptosis  complement activation  cobra venom factor  
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