同型半胱氨酸与白细胞黏附分子CD11b、CD18关系的体内外研究

Study of homocysteine level and CD11b/CD18 expressions on leukocytes in vivo and in vitro

目的研究探讨同型半胱氨酸(HCY)与炎性指标白细胞黏附分子CD11b/CD18之间的关系。方法体外研究:用免疫萤光流式细胞仪检测体外HCY和健康人血白细胞表面黏附分子CD11b、CD18的表达。体内研究:选择75例急性冠脉综合征(ACS)患者为ACS组,35例稳定性心绞痛(NACS)患者为NACS组,35名健康人为对照组。采用酶联免疫法测定血浆HCY水平,通过流式细胞仪采用直接免疫荧光法测定白细胞黏附分子CD11b/CD18的表达,同时对血浆C-反应蛋白(CRP)含量和白细胞计数等进行检测和分析。结果①HCY在体外明显增加CD11b和CD18在各种白细胞的表达,这种作用随HCY浓度升高而增强。②ACS组血浆HCY水平、平均白细胞表面黏附分子CD11b和CD18表达、CRP含量和白细胞计数显著高于NACS组和对照组(P<0.05)。③与对照组相比,稳定型心绞痛组仅HCY水平轻度升高,余差异无统计学意义。结论①同型半胱氨酸导致体外白细胞黏附分子的表达;ACS患者同型半胱氨酸、CD11b/CD18,C-反应蛋白含量和白细胞计数明显升高。②炎症可能是ACS发生的重要原因之一,同型半胱氨酸、白细胞、及其CD11b/CD18表达和CRP等共同参与了ACS的发生。

Objective To evaluate the plasma homocysteine level （HCY） and CDllb/CD18 expressions on leukocytes in vivo and in vitro. Methods The method of immunofluorescence flow cytometry was performed for measuring CDllb/CD18 expression on homocyteine treated leukocytes from the healthy subjects in vitro. Clinical study included 75 ACS patients, 35 stable coronary heart disease patients （NACS） and 35 healthy controls based on their clinical situations,electrocardiogram,cardiac enzyme,cTNT, and cardioangiography. Venous HCY level was measured by enzyme immunoassay and leukocyte surface adhesive molecule CDllb/CD18 expressions were analyzed by irmnunofluorescence flow cytometry. CRP, WBC and etc were also measured and analysed. Results （1） In vitro homocysteine at the concentration of 200 μmol/L significantly increased surface adhesive molecule expression of CDllb and CD18 on each cell type. （2） The levels of HCY, CDllb, CD18, CRP and WBC were markedly increased in ACS than those in NACS and controls （P〈0.05-0.01）. Despite of the high level of HCY in NACS, there was no difference of other parameters between NACS and controls. Conclusion （1） Homocysteine induced leukocyte expression of CDllb/CD18 on leukocytes in vitro, the levels of homocysteine, CDllb/CD18, CRP and WBC were higher in ACS group. （2）Inflammation may be one of important reasons for ACS occurrence and homocysteine, leukocytes and their CDllb/CD18 expressions and CRP were involved in the occurrence of ACS together.