中文摘要：

目的探讨心肌缺血再灌注后CXC趋化因子配体16（CXCL16）水平的变化及调节机制。方法将30只新西兰大白兔,按照随机数字表法分为假手术组、心肌缺血再灌注组和四氢吡咯二硫代氨基甲酯（PDTC）组。PDTC组经耳缘静脉注射20 mg/kg PDTC,30 min后PDTC组和心肌缺血再灌注组结扎冠状动脉,1.5 h后松解缝合线,假手术组只穿线不结扎。再灌注1 h后从左心房注入硫磺素S,无复流区无荧光着色;于原位重新结扎左回旋支,从左心房再次注入伊文斯蓝,非蓝染区域为缺血区。处死动物,沿平行房室沟方向将心室切片,手动描记心肌切片左心室壁、缺血区、无复流区轮廓。于动物结扎时和结扎后45、100、150 min时采用乙二胺四乙酸（EDTA）抗凝管自耳缘静脉采血5 ml,应用双抗体夹心酶标免疫分析法测定CXCL16水平。取左心室室间隔区、缺血区、无复流区心肌组织染色,以细胞核染阳性率反映心肌NF-κB p65表达水平。结果 PDTC组心肌缺血范围和无复流范围均小于心肌缺血再灌注组,差异有统计学意义（P〈0.05）。不同干预措施对动物结扎后不同时间CXCL16水平的影响,差异有统计学意义（P〈0.05）。心肌缺血再灌注组结扎后100 min CXCL16水平高于结扎时和结扎后45 min,差异有统计学意义（P〈0.05）。各组缺血区和无复流区细胞核染阳性率比较,差异均有统计学意义（P〈0.05）;其中,心肌缺血再灌注组缺血区和无复流区细胞核染阳性率高于假手术组和PDTC组,差异有统计学意义（P〈0.05）。结论心肌缺血再灌注可诱导CXCL16的表达;抑制NF-κB的激活可降低CXCL16的水平,缩小心肌缺血范围和无复流范围。

英文摘要：

Objective To investigate the change and regulation mechanism of the level of plasma CXC- chemokine ligand 16（ CXCL16）. Methods We divided 30 New Zealand white rabbits into 3 groups： sham- operation group,cardiac ischemia / reperfusion（ I / R） group and pyrrolidine dithiocarbamate（ PDTC） group. The PDTC group was administrated with 20 mg / kg PDTC by ear marginal vein injection,and 30 minutes later,the PDTC group and I / R group were administrated with coronary artery ligation; 1. 5 hours later,suture line was unbound; and the sham- operation group was only sutured without ligation. One hour after reperfusion,Thioflavine S was injected into atrium sinistrum,leaving no fluorescence staining in no reflow area. Ligation of left circumflex artery was made again at the primary site, and Evans blue was injected into atrium sinistrum again,with no blue stain area in ischemic area. After the animals were killed,ventricular slice was taken parallel to the atrioventricular groove,and the outlines of left ventricular wall,ischemic region and no reflow area were made manually on myocardial biopsy. During ligation,and 45 minutes,100 minutes and 150 minutes after ligation,ethylenediamine tetraacetic acid（ EDTA） anticoagulative tube was employed to sample 5 ml blood from ear marginal vein,and double antibody sandwich enzyme immunoassay was used to determine CXCL16 level. Myocardial tissue staining results of left ventricular septal area,ischemic region and no flow area were obtained,and the dyeing positive rate of cell nucleus was used to reflect the expression of NF-κB p65. Results The area of myocardial ischemia and the no- flow area of PDTC group were both smaller than I / R group（ P 〈0. 05）. Different intervention measures were significantly different in the influence on the level of CXCL16 at different time points（ P 〈0. 05）. In I / R group,the level of CXCL16 at 100 minutes after ligation was higher（ P 〈0. 05） than that during ligation and 45 minutes after ligation. The three groups wer