中文摘要：

目的：探讨丝裂原活化蛋白激酶（Mitogen-activated protein kinases,MAPKs）在anti-β2 GPI/β2 GPI复合物诱导单核细胞株THP-1表达组织因子（TF）中的活化及其作用。方法：利用荧光定量PCR（Real-time PCR）、TF活性试剂盒等分别检测anti-β2 GPI/β2 GPI复合物诱导THP-1细胞表达TF mRNA及TF活性,Western blot检测细胞表达p38、磷酸化-p38（p-p38）、ERK1/2、磷酸化-ERK1/2（p-ERK1/2）、JNK、磷酸化-JNK（p-JNK）的情况。进一步采用p38、ERK1/2、JNK抑制剂（SB203580、U0126、SP600125）观察是否能阻断anti-β2 GPI/β2 GPI复合物诱导THP-1细胞表达TF。结果：Anti-β2 GPI/β2 GPI复合物（100μg/ml）能够显著增强THP-1细胞表达TF,并使p-p38、p-ERK1/2、p-JNK水平显著升高（P〈0.05 vs control）;其引发的MAPKs磷酸化具有时间效应性,均在刺激30分钟时达到高峰;对应的特异抑制剂SB203580（10μmol/L）、U0126（5μmol/L）、SP600125（90 nmol/L）单独或合并处理THP-1细胞后,anti-β2 GPI/β2 GPI复合物诱导细胞TF mRNA表达及TF活性的效应明显被阻断（P〈0.01 vs control）。结论：Anti-β2 GPI/β2 GPI复合物诱导THP-1细胞表达TF过程中,MAPKs被激活进而发挥重要作用。

英文摘要：

Objective：To investigate whether mitogen-activated protein kinases（MAPKs） are involved in anti-β2 GPI/β2 GPI-induced tissue factor（TF） expression in THP-1 cells.Methods：TF expression in THP-1 cells was measured by Real-time PCR or TF activity after stimulating with anti-β2 GPI/β2 GPI complex.The activation of p38,ERK1/2,and JNK induced by anti-β2 GPI/β2 GPI complex were determined by Western blot using phosphor-specific antibodies.Inhibitors against p38,ERK1/2,JNK（SB203580,U0126,SP600125） were used to test whether the blockade of these pathway would interrupt the induction of TF expression in THP-1 cells by anti-β2 GPI/β2 GPI complex.Results：p38,ERK1/2,and JNK were active in a time-dependent manner in THP-1 cells upon treatment with anti-β2 GPI/β2 GPI complex（100 μg/ml）.Induction of TF mRNA expression and TF activity by anti-β2 GPI/β2 GPI complex（100 μg/ml） in THP-1 cells could be blocked by inhibitors against the MAPKs,SB203580（10 μmol/L）,U0126（5 μmol/L）,SP600125（90 nmol/L）.Conclusion：MAPKs can be activated by anti-β2 GPI/β2 GPI in THP-1 cells and is involved in the induction of TF expression.