中文摘要：

目的探讨p65小干扰RNA（siRNA）对人脐静脉内皮细胞再灌注损伤后趋化因子CXCL16表达的调节机制。方法分4组对人脐静脉内皮细胞进行培养和处理，即对照组（正常培养基培养）、缺血再灌注组（以模拟缺血培养液培养30min后换正常培养液再培养4h）、p65siRNA转染组（正常内皮细胞培养基培养＋p65siRNA转染）、缺血再灌注＋p65siRNA转染组（模拟缺血再灌注＋p65siRNA转染）。观察4组核因子KBv65、CXCL16mRNA相对表达量及CXCL16表达水平以及细胞存活率。结果对照组、p65siRNA转染组及缺血再灌注＋p65siRNA转染组核心子KBp65、CXCL16mRNA相对表达量及CXCL16表达水平较缺血再灌注组均降低（P〈0．05）。WST-1法测定，p65siRNA转染组及缺血再灌注’p65siRNA转染组细胞存活率较缺血再灌注组均增高（P〈0．05）。结论p65siRNA通过沉默p65，抑制模拟缺血再灌注诱导的CXCL16表达，有利于细胞生存。

英文摘要：

Objective To investigate the regulation mechanism of CXCL16 under the condition of mimic ischemia reperfusion in human umbilical vein endothelial cells （HUVEC） by utilizing p65 siRNA. Methods HUVEC were divided into 4 groups ： control group （ HUVEC were cultured with normal medium） , mimic ischemia reperfusion group （ HUVEC were cultured with mimic ischemic medium for 30 rain, then were cultured with normal medium for 4 h） , p65 siRNA group （ HUVEC were cultured with normal medium, and were transfeeted with p65 siRNA ）, mimic ischemia reperfusion ＋ p65 siRNA group （ HUVEC were transfeeted with p65 siRNA, 48 h later, HUVEC were cultured with mimic ischemia medium） . The relative ex- pression quantity of KB p65 and CXCL16 mRNA, the expression level of CXCL16 and cell survival rate were investigated. Results The expression quantity of KB p65 and CXCL16 and the expression level of CXCL16 in control group, p65 siRNA group and mimic ischemia reperfusion ＋ p65 siRNA group were significantly lower than those in mimic ischemia reperfusion group （ P 〈 0.05 ）. Meanwhile, by the method of WST - 1 assay, cell survival rate in p65 siRNA group and mimic ischemia reperfusion ＋ p65 siRNA group were significantly higher than that in mimic ischemia reperfusion group （ P 〈 0. 05 ） . Conclusion By silencing p65, p65 siRNA can inhibit mimic isehemic reperfusion - induced expression level of CXCL16, which brings benefits to the survival of HUVEC.