聚氨酯(PU)和聚四氟乙烯(PTFE)是两种常用的血液接触生物材料。该研究通过建立一个非接触的细胞共培养模型从而针对材料刺激血液单核细胞活化后诱导血栓的潜能进行评估。运用人脐静脉内皮细胞和人单核细胞系THP-1进行实验,首先将PU和PTFE与THP-1细胞直接接触,然后收集细胞上清液,用上清液培养人脐静脉内皮细胞,结果发现内皮细胞上调炎症趋化因子单核细胞趋化蛋白1(MCP-1),巨噬细胞炎症蛋白-1α(MIP-1α)的表达。为进一步探讨THP-1细胞在其中所起到的作用,用MTS试验研究细胞的增殖程度,用ELISA试验研究细胞所分泌的可溶性分子,结果发现这些材料能不同程度地刺激THP-1细胞增殖及活化,使其分泌细胞因子TNF-α及/或IL-1β。研究表明,与血液接触的生物材料可能通过作用于单核细胞,使其增殖及活化,分泌促炎症因子,使得内皮细胞发生炎性激活,最终导致血栓形成。
Polyurethane(PU) and polytetrafluorethylene(PTFE) are 2 commonly used blood-contacting biomaterials.In the present study,we used a noncontact coculture model to evaluate the thrombosis-causing potential of monocyte-mediated PU and PTFE.We used human endothelial cells from umbilical cord(HUVECs) and human monocytes(THP-1 cells).The THP-1 cells were directly exposed to PU/PTFE,and the resultant cell-free supernatants were harvested for stimulating HUVECs.The results demonstrated that both PU and PTFE induced the expressions of monocyte chemoattractant protein-1(MCP-1) and macrophage inflammatory protein-1α(MIP-1α) in HUVECs.To further investigate the role THP-1 cells played in the process,MTS assay was used to measure the THP-1 cell viability and ELISA was used to detected monocyte-derived soluble factors that might contribute to these effects.In comparison with the results for the negative control,both PU and PTFE variably induced THP-1 cell proliferation and activation,and subsequently caused the release of soluble factors TNF-α/ IL-1β.Our results suggest that the blood-contacting biomaterial induces monocytic proliferation and activation,which contribute to the release of proinflammatory factors and inflammatory activation in HUVECs,and finally cause thrombogenesis.