中文摘要：

目的探讨雷帕霉素靶蛋白（mTOR）在抗β2糖蛋白I（β2GPI）/β2GPI复合物诱导THP-1细胞组织因子（TF）表达中的作用。方法用抗β2GPI抗体/β2GPI和β2GPI/Ig G-APS处理THP-1细胞,mTOR抑制剂雷帕霉素（100 nmol/L）进行干预实验;收集细胞总RNA和蛋白质,实时定量PCR（RT-q PCR）和TF活性试剂盒分别检测THP-1细胞中TF mRNA表达水平及其活性,western blot检测THP-1细胞中mTOR、磷酸化mTOR（p-mTOR）、p38、p-p38、ERK1/2、p-ERK1/2、JNK、p-JNK、NF-κB p65和p-NF-κB p65的表达情况。结果抗β2GPI抗体/β2GPI和β2GPI/Ig G-APS复合物均能明显增加THP-1细胞TF mRNA和TF活性以及mTOR磷酸化水平（P均〈0.05）;雷帕霉素能明显降低抗β2GPI抗体/β2GPI和β2GPI/Ig G-APS诱导THP-1细胞TF的表达水平以及mTOR磷酸化的效应（P均〈0.05）,也能明显地削弱p38、ERK1/2和NF-κB p65的磷酸化水平（P均〈0.05）,而对JNK的磷酸化水平无抑制效应（P〉0.05）。结论抗β2GPI抗体/β2GPI复合物能够刺激THP-1细胞mTOR的活化,并能影响TF的表达。

英文摘要：

Objective To investigate the role of mammalian target of rapamycin （mTOR） in the expression of tissue factor （TF） from THP-1 cells induced by β2GPI/anti-β2GPIcomplex. Methods The THP-1 ceils were treated with both β2GPI/anti-β2GPI and β2GPI/IgG-APS（ β2GPI/IgG from APS patients） complexes. Rapamycin（ 100 nmol/L）, the mTOR inhibitor, was used to exert the intervention experiment. The total RNA and proteins of the THP-1 cells were collected for detection. The mRNA expression level and ac- tivity of TF in THP-1 cells were detected by real-time quatitative PCR（RT-qPCR） and TF activity kit respectively, western blot was used to determine the levels of mTOR and phosphorylated-mTOR（p-mTOR） , and p38, p-p38, ERK1/2, p-ERK1/2, JNK, p-JNK, NF-KB p65 and p-NF-KB p65 in THP-1 cells were determined simultaneously. Results Both β2GPI/anti-β2GPI and β2GPI/IgG-APS complexes chould significantly upregulate the mRNA expression and activity of TF, and the phosphorylation levels of roTOR in THP-1 cells（P 〈 0.05 ）. Rapamycin markedly attenuated the mRNA expression and activity of TF and mTOR phosphorylation induced by 132GPI/anti-β2GPI and [32GPI/IgG-APS complexes（P 〈 0.05）, and also inhibited the phosphorylation levels of p38, ERK1/2 and NF- KB p65 in THP-1 cells induced by 132 GPI/anti-β2 GPI and 132 GPI/IgG-APS complexes （P 〈 0.05）, but did not showed effects on the phosphorylation of c-Jun NH2-terminal protein kinase （JNK） （ P 〉 0.05 ）. Conclusion mTOR could be activated by β2 GPI/anti- β2GPI complexes in THP-1 cells and play a crucial role for β2GPI/anti-β2GPI-induced TF expression in THP-1 cells.