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目的 :研究尼古丁对人树突状细胞 (DC)功能的影响及其与急性冠状动脉综合征 (ACS)发病的关系。方法 :观察体外尼古丁对DC功能的作用以及 11例正常对照者 (正常对照组 )与 45例ACS者 (ACS组 )发病时及戒烟后DC的功能状态。流式细胞仪检测DCCD86的表达 ;混合淋巴反应检测DC对T淋巴细胞的刺激作用 ;酶联免疫吸附法 (ELISA)测定混合淋巴反应上清液中细胞因子水平。结果 :与正常对照组比较 ,ACS时DC表面CD86的表达明显增高 ,对T淋巴细胞刺激的能力增强 ;致炎细胞因子分泌增多 ;DCCD86的表达与日吸烟量正相关 (r =0 63 ,P <0 0 1) ;平均戒烟 5个月后 ,DC功能接近正常 ;体外尼古丁亦能明显刺激DC的功能 ,呈浓度依赖性。结论 :①ACS时DC明显激活 ;②戒烟后DC功能可迅速恢复 ;③尼古丁可能是ACS时DC激活的刺激因素之一。
Objective: To study the effect of nicotine on the function of human dendritic cells (DC) and its relationship with the pathogenesis of acute coronary syndrome (ACS). Methods: The effects of nicotine on DC function in vitro and the functional status of DC in 11 normal controls (control group) and 45 ACS patients (ACS group) were observed. Flow cytometry was used to detect the expression of DCCD86. The mixed lymphocyte reaction was used to detect the stimulatory effect of DC on T lymphocytes. The levels of cytokines in the mixed lymphatic response supernatant were measured by enzyme linked immunosorbent assay (ELISA). Results: Compared with the normal control group, the expression of CD86 on DC surface was significantly increased and the ability to stimulate T lymphocytes was enhanced; the secretion of inflammatory cytokines was increased; the expression of DCCD86 was positively correlated with the daily smoking (r = 0 63, P <0 0 1). After 5 months’ smoking cessation, DC function was close to normal. Nicotine in vitro also significantly stimulated the function of DC in a concentration-dependent manner. CONCLUSIONS: ① DC is activated obviously on ACS; ② DC function can be quickly recovered after quitting smoking; ③ Nicotine may be one of the stimulating factors of DC activation during ACS.