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[稳脉通对高脂血症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].

作者信息

Hao Yu, Hang Xiao-tong, Jia De-xian

机构信息

Beijing University of Chinese Medicine, Beijing.

出版信息

Zhongguo Zhong Xi Yi Jie He Za Zhi. 2007 Apr;27(4):335-8.

Abstract

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.

摘要

目的

研究温脉通及其拆方对高脂血症血清诱导的单核细胞与内皮细胞黏附的影响,探讨温脉通治疗早期动脉硬化闭塞症(ASO)的作用机制。

方法

分别常规制备含温脉通全方及其拆方(包括温经益气部分即温经益气方、活血化瘀部分即活血通脉方)的血清以及高脂血清。采用孟加拉玫瑰红染色法检测单核细胞株THP-1与人脐静脉血管内皮细胞(HUVEC)的黏附情况,并用ELISA法检测HUVEC表面细胞间黏附分子(ICAM-1)、血管细胞黏附分子(VCAM-1)及P-选择素的表达。

结果

温脉通可抑制高脂血症血清诱导的THP-1与HUVEC的黏附,并下调HUVEC表面ICAM-1、VCAM-1、P-选择素的表达,两方拆方可下调不同的黏附分子。

结论

温脉通治疗ASO的机制之一可能是通过下调血管内皮细胞黏附分子的表达,减少单核细胞与血管内皮细胞的黏附,从而抑制单核细胞迁入血管内膜形成泡沫细胞,进而抑制动脉硬化。

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