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Titolo:
Shikonin, a component of antiinflammatory Chinese herbal medicine, selectively blocks chemokine binding to CC chemokine receptor-1
Autore:
Chen, X; Oppenheim, J; Howard, OMZ;
Indirizzi:
NCI, Frederick Canc Res & Dev Ctr, Div Basic Sci, Mol Immunoregulat Lab, Frederick, MD 21701 USA NCI Frederick MD USA 21701 Mol Immunoregulat Lab, Frederick, MD 21701 USA
Titolo Testata:
INTERNATIONAL IMMUNOPHARMACOLOGY
fascicolo: 2, volume: 1, anno: 2001,
pagine: 229 - 236
SICI:
1567-5769(200102)1:2<229:SACOAC>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMALL-MOLECULE ANTAGONIST; IDENTIFICATION; ACETYLSHIKONIN; NEUTROPHILS; INHIBITION; POTENT;
Keywords:
CCR1; receptor binding; shikonin; antagonist;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Howard, OMZ NCI, Frederick Canc Res & Dev Ctr, Div Basic Sci, Mol Immunoregulat Lab, Frederick, MD 21701 USA NCI Frederick MD USA 21701 gulat Lab, Frederick, MD 21701 USA
Citazione:
X. Chen et al., "Shikonin, a component of antiinflammatory Chinese herbal medicine, selectively blocks chemokine binding to CC chemokine receptor-1", INT IMMUNO, 1(2), 2001, pp. 229-236

Abstract

Shikonin is a chemically characterized component of traditional Chinese herbal medicine and has been shown to possess antiinflammatory activities. Weascertained that shikonin blocked radiolabelled Regulated on Activation, Normal T cell Expressed and Secreted (RANTES) and macrophage inflammatory protein-1 (MIP-1 alpha) binding to human monocytes with IC50 values of 3.58 x10(-6) and 2.57 X 10(-6) M, respectively. In contrast, up to 1.7 X 10(-5) M of shikonin failed to inhibit stromal cell-derived factor-1 (SDF-1 alpha )binding to the cells. Additionally, shikonin blocked RANTES and MIP-1 alpha binding to stable CC chemokine receptor-1 (CCR1) transfected human embryonic kidney (HEK)/293 cells with IC50 values of 2.63 x 10(-6) and 2.57 X 10-6 M, respectively. However, shikonin inhibited neither RANTES nor MIP-1 alpha binding to CCR5 transfected HEK/293 cells. Shikonin also did not inhibitmonocyte chemoattractant protein-1 (MCP-1) binding to CCR2 cells, eotaxin binding to CCR3 cells, interferon-inducible T cell alpha -chemoattractant (1-TAC) binding to CXCR3 cells and SDF-1 alpha binding to CXCR4 cells. Additionally, shikonin inhibited RANTES-induced CCR1 cell migration, but did notinhibit CCR1 cell migration induced by epidermal growth factor (EGF). Our study suggests shikonin may be a target for the future design of more potent, highly selective therapeutics that could be useful antiinflammatory agents far selectively blocking the binding of CCR1 ligands. (C) 2001 Publishedby Elsevier Science B.V.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 20:26:08