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聚氨酯促肿瘤活性的研究:聚亚烷基聚氨酯而非聚醚聚氨酯表面代谢协同抑制作用的耗竭。

Studies on the tumor-promoting activity of polyurethanes: depletion of inhibitory action of metabolic cooperation on the surface of a polyalkyleneurethane but not a polyetherurethane.

作者信息

Tsuchiya T, Takahara A, Cooper S L, Nakamura A

机构信息

Division of Medical Devices, National Institute of Health Sciences, Tokyo, Japan.

出版信息

J Biomed Mater Res. 1995 Jul;29(7):835-41. doi: 10.1002/jbm.820290708.

DOI:10.1002/jbm.820290708
PMID:7593022
Abstract

Methanol extracts prepared from three polyetherurethanes (PEUs), namely PU4, PU6, and PU8, which were synthesized using 4,4'-diphenylmethanediisocyanate, poly(tetramethylene oxide), and 1,4-butanediol, showed an inhibitory action on the gap-junctional intercellular communication in a V79 metabolic cooperation (MC) test system. However, the inhibitory potentials of methanol extracts did not correlate with the tumorigenic potential of the polyurethanes in 1-year rat implantation studies. When the MC test was carried out using glass dishes partly coated with low molecular weight PEU, the inhibitory activity was clearly detected on the surface of the polyurethane coating but not on that of the noncoated glass area. The inhibitory activity of the three PEUs investigated using polyurethane-coated dishes correlated with the values of the polyurethane's tumorigenic potential in the rat implantation study. Various polyurethanes containing polybutadiene (PBD), hydrogenated polybutadiene (HPBD), or a fluoropolyether glycol (FPEG) as the soft segment were also tested using coated dishes in the MC assay. The threshold inhibitory response of FPEG-PU was 10-fold less than that of PU4, and neither PBD-PU nor HPBD-PU showed any inhibition in the MC test system. Both the FPEG and aliphatic soft segment containing polyurethanes decreased, and had minimal influence on the gap junctional intercellular communication. Thus, the tumor-promoting potential of PBD-PU, HPBD-PU, and FPEG-PU was considered to be lower than those of the PEUs based on these in vitro test results.

摘要

由三种聚醚聚氨酯(PEU),即PU4、PU6和PU8制备的甲醇提取物,在V79代谢合作(MC)测试系统中显示出对间隙连接细胞间通讯的抑制作用。这三种聚醚聚氨酯是使用4,4'-二苯基甲烷二异氰酸酯、聚四氢呋喃和1,4-丁二醇合成的。然而,在为期1年的大鼠植入研究中,甲醇提取物的抑制潜力与聚氨酯的致瘤潜力并不相关。当使用部分涂有低分子量PEU的玻璃培养皿进行MC测试时,在聚氨酯涂层表面能清楚地检测到抑制活性,而在未涂层的玻璃区域则未检测到。使用聚氨酯涂层培养皿研究的三种PEU的抑制活性与大鼠植入研究中聚氨酯的致瘤潜力值相关。还使用涂层培养皿在MC试验中测试了各种含有聚丁二烯(PBD)、氢化聚丁二烯(HPBD)或含氟聚醚二醇(FPEG)作为软段的聚氨酯。FPEG-PU的阈值抑制反应比PU4低10倍,并且PBD-PU和HPBD-PU在MC测试系统中均未显示出任何抑制作用。含FPEG和脂肪族软段的聚氨酯均降低了间隙连接细胞间通讯,且对其影响最小。因此,基于这些体外测试结果,认为PBD-PU、HPBD-PU和FPEG-PU的促肿瘤潜力低于PEU。

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Studies on the tumor-promoting activity of polyurethanes: depletion of inhibitory action of metabolic cooperation on the surface of a polyalkyleneurethane but not a polyetherurethane.聚氨酯促肿瘤活性的研究:聚亚烷基聚氨酯而非聚醚聚氨酯表面代谢协同抑制作用的耗竭。
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引用本文的文献

1
A strategy for the suppression of tumorigenesis induced by biomaterials: Restoration of transformed phenotype of polyetherurethane-induced tumor cells by Cx43 transfection.一种抑制生物材料诱导肿瘤发生的策略:通过 Cx43 转染恢复聚醚型聚氨酯诱导的肿瘤细胞的转化表型。
Cytotechnology. 2002 May;39(1):1-8. doi: 10.1023/A:1022430021868.