低剂量FasL诱导bEnd.3细胞增殖及机制研究
张春兵;张明顺;滕凤猛;高峰
【期刊名称】《南京中医药大学学报》 【年(卷),期】2013(029)004
【摘要】目的 探讨低剂量FasL诱导小鼠脑微血管内皮细胞bEnd.3增殖及其可能机制.方法 以500～0.015 6 ng/mL 1/2倍比稀释共9个浓度梯度FasL干预bEnd.3细胞培养48 h,CCK-8检测bEnd.3细胞增殖能力,ELISA检测bEnd.3细胞分泌表达VEGF能力,RNAi抑制Fas表达,Western blotting检测FADD、FLIP、TRAF蛋白表达水平,EMSA检测NF-κB蛋白表达水平.结果 0.156 ng/mL FasL干预bEnd.3细胞,可诱导细胞增殖明显增加(P＜0.05),bEnd.3细胞分泌表达VEGF能力明显增加(P＜0.05),F(A)DD、FLIP、TRAF、NF-κB蛋白表达水平明显增加(P＜0.05)；RNAi抑制Fas基因后,细胞增殖无明显变化(P＞0.05),FADD、FLIP、TRAF蛋白表达水平明显下降(P＜0.05),NF-κB蛋白表达水平无明显变化(P＞0.05).结论 低剂量FasL可诱导bEnd.3细胞增殖,FADD-FLIP-TRAF-NF-κB信号传导途径是其机制之一.%OBJECTIVE To investigate the proliferation and possible mechanism of rat's cerebral microvascular endothelial cells induced by low dose FasL.METHODS 9 FasL of different concentration gradients was diluted 500～0.015 6 ng/mL 1/2multiple proportion and the cell culture of bEnd.3 was interfered by 48 h.The cell proliferation ability of bEnd.3 was tested by CCK-8.The VEGF cell secreted expression ability of bEnd.3 was tested by ELISA.Fas Expression was inhibited by RNAi.The protein express levels of FADD,FLIP and TRAF
低剂量FasL诱导bEnd.3细胞增殖及机制研究
