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郝钰,杭小同,贾德贤,葛辛,邱全瑛,陈淑长.温脉通对高脂血清诱导的单核细胞与血管内皮细胞黏附的影响[J].,2007,(4):335-338
温脉通对高脂血清诱导的单核细胞与血管内皮细胞黏附的影响
Effect of Wenmaitong on Adhesion of Monocytes to Vascular Endothelial Cell Induced by Hyperlipidemic Serum
  
DOI:
中文关键词:  温脉通  动脉硬化闭塞症  高脂血清  黏附分子
英文关键词:Wenmaitong  arteriosclerosis obliterans  hyperlipidemic serum  adhesion molecules
基金项目:国家自然科学基金资助项目(No30371792)
Author NameAffiliation
HAO Yu 北京中医药大学基础医学院 
HANG Xiao-tong 北京中医药大学基础医学院 
JIA De-xian 北京中医药大学基础医学院 
葛辛 北京中医药大学东方医院 
邱全瑛 北京中医药大学基础医学院 
陈淑长 北京中医药大学东方医院 
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中文摘要:
      目的研究温脉通及其拆方对高脂血清诱导的单核细胞与血管内皮细胞黏附及黏附分子表达的影响,以探讨温脉通治疗早期动脉硬化闭塞症(ASO)的机制。方法常规制备温脉通全方、温经益气拆方、活血通脉拆方含药血清和高脂血清,采用虎红染色法检测药物血清对高脂诱导的人脐静脉内皮细胞(HU-VEC)和单核细胞株(THP-1)黏附的作用;用细胞ELISA法检测HUVEC表面细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)、P-选择素(P-selectin)的表达。结果温脉通能抑制高脂诱导的HUVEC与THP-1的黏附,并下调HUVEC表面ICAM-1、VCAM-1、P-selectin的表达;两拆方组对不同的黏附分子有下调作用。结论下调血管内皮细胞黏附分子的表达,减少单核细胞与内皮细胞的黏附,从而抑制单核细胞迁移至血管内膜形成泡沫细胞,抑制动脉粥样硬化(AS)的形成,可能是温脉通治疗ASO的机制之一。
英文摘要:
      Objective To study the effect of Wenmaitong (WMT) and its disassembled formulas on the adhesion of monocytes to endothelial cells induced by hyperlipidemic serum to explore the mechanism of WMT on early arteriosclerosis obliterans (ASO). Methods Serums containing whole WMT and its disassembled formulas, including the formula consisted of warming Jing and boosting qi part (Wenjin Yiqi, WY) and that of promoting blood circulation part (Huoxue Tongmai, HT), as well as the serum contained high concentration of lipids were prepared conventionally, respectively. The adhesion of monocytes cell strain THP-1 to human umbilical vascular endothelial cells (HUVEC) was determined by rose bengal stain method, and ELISA was used to detect expressions of intercellular adhesion molecule (ICAM-1), vascular cellular adhesion molecule (VCAM-1) and P-selectin on HUVEC surface. Results WMT could inhibit THP-1 to HUVEC adhesion induced by hyperlipidemic serum, and down-regulate the expression of ICAM-1, VCAM-1, P-selectin on HUVEC surface, the two disassembled formulas could down-regulate different adhesion molecules. Conclusion One mechanism of WMT on ASO may be its inhibition on arteriosclerosis by way of down-regulating the expression of vascular endothelial cells adhesion molecules to decrease the adhesion of monocyte to VEC, therefore to inhibit the monocytes migrating into vascular intima to develop foam cells.
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