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Iron tetrakis (N-methyl-4′-pyridyl) porphyrinato inhibits proliferative activity of thymocytes by blocking activation of p38 mitogen-activated protein kinase, nuclear factor-κB, and interleukin-2 secretion

Title
Iron tetrakis (N-methyl-4′-pyridyl) porphyrinato inhibits proliferative activity of thymocytes by blocking activation of p38 mitogen-activated protein kinase, nuclear factor-κB, and interleukin-2 secretion
Authors
Kang J.L.Lee H.S.Jung H.J.Kim H.J.
Ewha Authors
이지희
SCOPUS Author ID
이지희scopus
Issue Date
2003
Journal Title
Toxicology and Applied Pharmacology
ISSN
0041-008XJCR Link
Citation
vol. 191, no. 2, pp. 147 - 155
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Iron tetrakis (N-methyl-4′-pyridyl) porphyrinato (FeTMPyP) has been demonstrated to be a potent scavenger of reactive oxygens and to have antiinflammatory activities. However, the effects of FeTMPyP on the function of T cells have not been illustrated. The objective of this study was to determine whether treatment of thymocytes with FeTMPyP inhibited the proliferative activity in response to various mitogens and, if so, to further characterize the mechanism of FeTMPyP immune modulation. The results indicate that treatment of thymocytes with FeTMPyP resulted in dose-dependent inhibition of thymocyte proliferation stimulated by concanawalin (Con) A-, Interleukin (IL)-1β; or lipopdy socchande-exposed macrophage supernatant. FeTMPyP treatment also inhibited Con A- or IL-1β-induced DNA-binding activity of NF-κB and IL-2 secretion by thymocytes. Both the p38 MAP kinase inhibitor SB203580 and the extracellular signal-regulated protein kinases inhibitor PD98059 blocked proliferative activity in Con A-stimulated thymocytes, while SB203580 but not PD98059 blocked nuclear factor (NF)-κB activation. FeTMPyP inhibited the activation and phosphorylation of p38 mitogen-activated protein kinase (MAPK) in response to Con A. These data suggest that FeTMPyP downregulates the proliferative activity by inhibition of p38 MAPK activation, NF-κB activation, and IL-2 secretion during mitogenic stimulation of thymocytes. Therefore, further studies concerning the effects of FeTMPyP on the human diseases associated with both inflammatory disorders and immunologic overactivation are warranted. © 2003 Elsevier Inc. All rights reserved.
DOI
10.1016/S0041-008X(02)00044-3
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의학전문대학원 > 의학과 > Journal papers
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