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硫酸酯聚糖与血管损伤后的新生内膜增厚有关。

Sulfatides are associated with neointimal thickening after vascular injury.

机构信息

Department of Cardiovascular Medicine, Dokkyo Medical University, 880 Kitakobayashi, Mibu, Tochigi, 321-0293 Japan.

出版信息

Atherosclerosis. 2010 Jul;211(1):291-6. doi: 10.1016/j.atherosclerosis.2010.01.033. Epub 2010 Feb 2.

DOI:10.1016/j.atherosclerosis.2010.01.033
PMID:20176357
Abstract

BACKGROUND

Sulfatides are known to be a native ligand of P-selectin. Platelet-leukocyte interaction via the cross-talk between P-selectin and Mac-1 (CD11b/CD18) plays an important role in the mechanism of neointimal thickening after vascular injury such as that seen in post-stent restenosis. However, the roles of sulfatides on restenosis have not been elucidated.

METHODS

Serum sulfatide levels, P-selectin expression on the surface of platelets, and activated Mac-1 on the surface of neutrophils were serially measured using both coronary sinus and peripheral blood samples in 21 patients who underwent coronary stent implantation.

RESULTS

The trans-cardiac gradient (coronary sinus minus peripheral blood) of the sulfatide levels significantly increased at 15 min (-1.47+/-2.87 to 0.59+/-1.44 nmol/ml, p<0.001), compared to baseline levels. The maximum response of the trans-cardiac gradient of P-selectin expression on the surface of platelets at 15 min after stent implantation (R=0.55, p<0.01), and that of activated Mac-1 on the surface of neutrophils at 48 h (R=0.59, p<0.01), were both positively correlated with that of serum sulfatide levels at 15 min. The angiographic late lumen loss was correlated with the trans-cardiac gradient of sulfatide levels at 15 min (R=0.48, p<0.05), platelet P-selectin expression at 15 min (R=0.42, p<0.05) and activated neutrophil Mac-1 expression at 48 h (R=0.46, p<0.05), but not with values at other sampling points.

CONCLUSIONS

Sulfatides may play a physiological role on inflammation in vascular injury and the development of neointimal thickening.

摘要

背景

硫酸软骨素是已知的 P-选择素的天然配体。血小板-白细胞通过 P-选择素和 Mac-1(CD11b/CD18)之间的串扰相互作用在血管损伤后的新生内膜增厚机制中发挥重要作用,例如支架内再狭窄后。然而,硫酸软骨素在再狭窄中的作用尚未阐明。

方法

在 21 名接受冠状动脉支架植入术的患者中,连续测量冠状动脉窦和外周血样本中血清硫酸软骨素水平、血小板表面 P-选择素表达和中性粒细胞表面活化 Mac-1。

结果

与基线水平相比,硫酸软骨素水平的跨心梯度(冠状动脉窦减去外周血)在 15 分钟时显著增加(-1.47+/-2.87 至 0.59+/-1.44 nmol/ml,p<0.001)。支架植入后 15 分钟血小板表面 P-选择素表达的跨心梯度最大反应(R=0.55,p<0.01)和 48 小时中性粒细胞表面活化 Mac-1 的最大反应(R=0.59,p<0.01)均与 15 分钟时血清硫酸软骨素水平呈正相关。血管造影晚期管腔丢失与 15 分钟时的跨心梯度硫酸软骨素水平(R=0.48,p<0.05)、15 分钟时血小板 P-选择素表达(R=0.42,p<0.05)和 48 小时时中性粒细胞活化 Mac-1 表达(R=0.46,p<0.05)相关,但与其他采样点的值无关。

结论

硫酸软骨素可能在血管损伤和新生内膜增厚的炎症中发挥生理作用。

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