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dc.contributor.authorLi, Chi-Hanen_US
dc.contributor.authorLee, Ru-Pingen_US
dc.contributor.authorLin, Yu-Lingen_US
dc.contributor.authorLin, Chen-Sien_US
dc.contributor.authorHsu, Bang-Geeen_US
dc.contributor.authorTseng, Feng-Jenen_US
dc.contributor.authorChen, Yu-Chengen_US
dc.contributor.authorLiao, Kuang-Wenen_US
dc.contributor.authorYang, Fwu-Linen_US
dc.date.accessioned2014-12-08T15:38:25Z-
dc.date.available2014-12-08T15:38:25Z-
dc.date.issued2010-12-01en_US
dc.identifier.issn1043-4666en_US
dc.identifier.urihttp://dx.doi.org/10.1016/j.cyto.2010.08.001en_US
dc.identifier.urihttp://hdl.handle.net/11536/26308-
dc.description.abstractPropofol anesthesia and sedation are known to downregulate the functions of many hematopoietic cells, such as macrophages and neutrophils, in vivo. However, the effects of propofol on secretion of the regulatory cytokine transforming growth factor beta 1 (TGF-beta 1) in vivo are unknown. In this study, the effects of propofol on TGF-beta 1 expression in human peripheral blood mononuclear cells, umbilical vein endothelial cells (HUVECs), lymphocytes (Jurkat) and monocytes (THP-1) were tested. Moreover, these sera were also tested for regulatory activity on monocyte endocytosis with or without treatment with the TGF-beta 1 pathway inhibitor SB431542. Propofol raised levels of both total and activated TGF-beta 1 in propofol-treated patient sera after surgical operations. Furthermore, propofol induced secretion of latent TGF-beta 1 in HUVEC cells and enhanced TGF-beta 1 activation in THP-1 and Jurkat cells in vitro. Additionally, sera from propofol-treated patients suppressed monocyte endocytosis ex vivo, an effect that was abrogated by the TGF-beta 1 pathway inhibitor SB431542. (C) 2010 Elsevier Ltd. All rights reserved.en_US
dc.language.isoen_USen_US
dc.subjectPropofolen_US
dc.subjectTGF-beta 1en_US
dc.subjectEndothelial cellsen_US
dc.subjectMonocytesen_US
dc.subjectImmunosuppressionen_US
dc.titleThe treatment of propofol induced the TGF-beta 1 expression in human endothelial cells to suppress endocytosis activities of monocytesen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.cyto.2010.08.001en_US
dc.identifier.journalCYTOKINEen_US
dc.citation.volume52en_US
dc.citation.issue3en_US
dc.citation.spage203en_US
dc.citation.epage209en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.department分子醫學與生物工程研究所zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.contributor.departmentInstitute of Molecular Medicine and Bioengineeringen_US
dc.identifier.wosnumberWOS:000284819300011-
dc.citation.woscount2-
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