Suppression of the inflammatory response from adherent cells on phospholipid polymers
The expression of interleukin‐1β (IL‐1β) messenger RNA (mRNA) in macrophage‐like cells cultured on phospholipid polymers was evaluated to determine the extent of the inflammatory response. As phospholipid polymers, poly(2‐methacryloyloxyethyl phosphorylcholine(MPC)‐co‐n‐butyl methacrylate(BMA)s (PMB...
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Veröffentlicht in: | Journal of biomedical materials research 2003-03, Vol.64A (3), p.411-416 |
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Sprache: | eng |
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Zusammenfassung: | The expression of interleukin‐1β (IL‐1β) messenger RNA (mRNA) in macrophage‐like cells cultured on phospholipid polymers was evaluated to determine the extent of the inflammatory response. As phospholipid polymers, poly(2‐methacryloyloxyethyl phosphorylcholine(MPC)‐co‐n‐butyl methacrylate(BMA)s (PMBs) were synthesized. Poly(ethylene terephthalate) (PET), poly(2‐hydroxyethyl methacrylate) (PHEMA), and segmented poly(ether urethane) (Tecoflex® 60) were used as reference biomedical polymers. The protein adsorption onto the polymer surfaces from a cell culture medium was determined. The amount of the total protein adsorbed onto the PMBs was lower than that adsorbed onto the reference polymers, and the amount of adsorbed protein decreased with an increase in the MPC units in the PMBs. Human premyelocytic leukemia cell line (HL‐60) was used, and the expression of IL‐1β mRNA was investigated with the reverse transcription polymerase chain reaction (RT‐PCR) method. When HL‐60 cells were cultured on PMBs, the expression of IL‐1β mRNA in the cells was much less than that on the reference polymers. In particular, the expression of IL‐1β mRNA in HL‐60 cells cultured on the PMBs containing more than 10 mol % MPC units was not detected. This corresponded to the reduced amount of adsorbed proteins on the PMB surfaces. These results suggest that the PMBs effectively suppressed the activation and inflammatory response of adherent macrophagelike cells. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res 64A: 411–416, 2003 |
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ISSN: | 1549-3296 0021-9304 1552-4965 1097-4636 |
DOI: | 10.1002/jbm.a.10433 |