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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 45 (1996), S. 224-229 
    ISSN: 1420-908X
    Keywords: E-selectin ; Intercellular adhesion molecule-1 ; Vascular cell adhesion molecule-1 ; Vascular endothelial cells ; Azaindolidine derivative
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stimulation of cultured human umbilical vein endothelial cells (HUVEC) with lipopolysaccharide (LPS) induces adherences for human promyelocytic cell line HL60. Adherence of HL60 cells to HUVEC stimulated with LPS for 4h was completely inhibited by pretreatment with SJC13, an azaindolidine derivative. The mechanism whereby SJC13 inhibits the adhesiveness of HUVEC was investigated. Pretreatment of SJC13 inhibited LPS-induced expression of E-selectin and vascular cell adhesion molecule-1 (VCAM-1), but not intercellular adhesion molecule-1 (ICAM-1), in HUVEC, determined by flow cytometry and cellular enzyme-linked immunosorbent assay (cell-ELISA). The inhibitory activity was concentration dependent between 62.5 and 1,000 μg/ml. SJC13 also selectively inhibited LPS-induced increases in E-selectin and VACM-1 mRNAs, indicating that the action of SJC13 is to inhibit synthesis of these molecules. These data demonstrate that SJC13 is capable of selectively inhibiting the expression of E-selectin and VCAM-1, but not ICAM-1, in endothelial cells.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 45 (1996), S. 448-451 
    ISSN: 1420-908X
    Keywords: Septic shock ; Neutrophil ; Cell adhesion molecule inhibitor ; Azaindolidine derivative ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An azaindolidine derivative, SJC13, selectively inhibits expression and mRNA synthesis of E-selectin and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVEC) stimulated with lipopolysaccharide (LPS). The present experiments were performed to determine the in vivo effects of SJC13 against the lethality of LPS. In a mouse model of septic shock, intravenous administration of SJC13 5 min prior to LPS injection prevented significantly the lethality at doses of 3 mg/kg and 10 mg/kg. The prophylactic effect was dose-dependent. When injected up to 1h after LPS injection, SJC13 inhibited significantly the lethality. Neutrophil emigration into lung tissues during sepsis induced with LPS, as assessed by lung myeloperoxidase (MPO) content and histological examination, was significantly prevented by SJC13 administration. These data demonstrate that SJC13 has therapeutic anti-inflammation potential in vivo.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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