Anti-atherosclerotic function of Astragali Radix extract: downregulation of adhesion molecules in vitro and in vivo.
Anti-atherosclerotic function of Astragali Radix extract: downregulation of adhesion molecules in vitro and in vivo.
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黄芪提取物的抗动脉粥样硬化功能：体内外粘附分子的下调
DOI：
10.1186/1472-6882-12-54
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发表时间：
2012-04-26
影响因子：
--
通讯作者：
Han YL
中科院分区：
文献类型：
--
作者：
You Y;Duan Y;Liu SW;Zhang XL;Zhang XL;Feng JT;Yan CH;Han YL
动脉粥样硬化被认为是一种慢性炎症性疾病。黄芪提取物(ARE)是从黄芪中提取的主要有效成分之一。虽然ARE具有抗炎作用，但其抗动脉粥样硬化的作用和机制尚未阐明。在肿瘤坏死因子-α诱导前，用不同剂量的ARE在不同时间对小鼠内皮细胞SVEC4-10进行预处理。采用THP-1细胞进行细胞黏附实验，用酶联免疫吸附试验、免疫印迹和免疫荧光分析检测血管细胞黏附分子-1、细胞间黏附分子-1、磷酸化κB抑制因子(p-IκB)和核因子-κB的表达，并观察ARE对载脂蛋白E基因缺陷(apoE−/−)小鼠动脉内皮细胞粥样硬化的影响。肿瘤坏死因子-α显著增加血管细胞间黏附分子-1和细胞间黏附分子-1的表达，并伴有p-IκB和NF-κB蛋白的表达增加。但ARE对血管细胞间黏附分子-1和细胞间黏附分子-1的表达均呈剂量和时间依赖关系，其中以120 μg/ml作用4 h的作用最强，同时伴有p-IκB表达的显著降低和对NF-κB活化的抑制。免疫荧光分析还显示，口服ARE可导致apoE−/−小鼠主动脉内皮细胞黏附分子表达下调，巨噬细胞表达减少。ARE可抑制apoE−/−小鼠的炎症反应，抑制动脉粥样硬化病变的进展。本研究表明ARE可能是一种治疗动脉粥样硬化的有效抗炎药，其作用机制可能与减少黏附分子的表达有关。
Atherosclerosis is considered to be a chronic inflammatory disease. Astragali Radix extract (ARE) is one of the major active ingredients extracted from the root of Astragalus membranaceus Bge. Although ARE has an anti-inflammatory function, its anti-atherosclerotic effects and mechanisms have not yet been elucidated. Murine endothelial SVEC4-10 cells were pretreated with different doses of ARE at different times prior to induction with tumor necrosis factor (TNF)-α. Cell adhesion assays were performed using THP-1 cells and assessed by enzyme-linked immunosorbent assay, western blotting and immunofluorescence analyses to detect the expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), phosphorylated inhibitor of κB (p-iκB) and nuclear factor (NF)-κB. We also examined the effect of ARE on atherosclerosis in the aortic endothelium of apolipoprotein E-deficient (apoE−/−) mice. TNF-α strongly increased the expression of VCAM-1 and ICAM-1 accompanied by increased expression of p-iκB and NF-κB proteins. However, the expression levels of VCAM-1 and ICAM-1 were reduced by ARE in dose- and time-dependent manners, with the strongest effect at a dose of 120 μg/ml incubated for 4 h. This was accompanied by significantly decreased expression of p-iκB and inhibited activation of NF-κB. Immunofluorescence analysis also revealed that oral administration of ARE resulted in downregulation of adhesion molecules and decreased expression of macrophages in the aortic endothelium of apoE−/− mice. ARE could suppress the inflammatory reaction and inhibit the progression of atherosclerotic lesions in apoE−/− mice. This study demonstrated that ARE might be an effective anti-inflammatory agent for the treatment of atherosclerosis, possibly acting via the decreased expression of adhesion molecules.
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DOI：
10.1161/01.atv.14.1.133
发表时间：
1994-01-01
期刊：
ARTERIOSCLEROSIS AND THROMBOSIS
影响因子：
--
作者：
NAKASHIMA, Y;PLUMP, AS;ROSS, R
通讯作者：
ROSS, R
影响因子：
15.9
作者：
MONTEFORT, S;GRATZIOU, C;CARROLL, MP
通讯作者：
CARROLL, MP
影响因子：
7.2
作者：
Xu, Xiao-Le;Ji, Hui;Cheng, Yan-Ping
通讯作者：
Cheng, Yan-Ping
DOI：
10.1358/mf.2009.31.2.1353846
发表时间：
2009-03-01
影响因子：
--
作者：
Han, D. -O.;Lee, H. -J.;Hahm, D. -H.
通讯作者：
Hahm, D. -H.
影响因子：
5.4
作者：
Ryu, Minsook;Kim, Eun Hye;Lee, Jong-Soo
通讯作者：
Lee, Jong-Soo