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  • 1
    Electronic Resource
    Electronic Resource
    Regulation of nitric oxide and prostaglandin E2 production by CSAIDSTM (SB203580) in murine macrophages and bovine chondrocytes stimulated with LPS (1999)
    Springer
    Inflammation research 48 (1999), S. 337-343 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Nitric oxide — Prostaglandin E2— p38 Kinase — Macrophages — Chondrocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective and Design: To compare two anti-inflammatory drugs: CSAIDSTM (SB 203580) and hydrocortisone on iNOS and COX-2 expression.¶Material or Subjects: Murine macrophages and bovine chondrocytes stimulated with LPS and human OA-affected cartilage were used in this study.¶Treatment: The macrophages and chondrocytes were preincubated (30 min) with 0.1-1.0 μM CSAIDSTM or 10 μM of hydrocortisone before stimulating them with 1-100 μg/ml LPS.¶Methods: The end products of iNOS and COX-2: nitric oxide (NO) and PGE2 were estimated by Greiss method and RIA, respectively.¶Results: CSAIDSTM (1 μM) inhibited the production of NO and PGE2 (p ≤ 0.01) in bovine chondrocytes, but not in murine macrophages (RAW 264.7) (p ≤ 0.1). In fact, CSAIDSTM (in murine macrophages) marginally augmented nitrite accumulation (∼ 20%) at 14-24 h of LPS stimulation. Western blot analysis of COX-2 in bovine chondrocytes show decrease in COX-2 expression by hydrocortisone but not CSAIDSTM, although hydrocortisone and CSAIDSTM inhibit PGE2 accumulation. Hydrocortisone inhibited both PGE2 and NO production significantly (p ≤ 0.01) in murine macrophages. Furthermore, hydrocortisone significantly inhibited (p ≤ 0.01) PGE2 but marginally (p ≤ 0.05) NO in bovine chondrocytes.¶Conclusion: These experiments demonstrate differential action of CSAIDSTM and hydrocortisone on NO and PGE2 production in bovine chondrocytes and RAW 264.7 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050469
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    The pleiotropic functions of aspirin: mechanisms of action (1999)
    Springer
    Cellular and molecular life sciences 56 (1999), S. 305-312 
    Details
    ISSN: 1420-9071
    Keywords: Key Words. Aspirin; prostaglandin; COX; signal transduction; NF-κB; NOS.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Recent studies have suggested that aspirin and aspirin-like compounds have a variety of actions in addition to their well-studied ability to inhibit cyclooxygenases. These actions include inhibition of the uncoupling of oxidative phosphorylation, decreases in adenosine triphosphate stores, increases in extracellular adenosine, downregulation of the expression and activity of inducible nitric oxide synthetase, inhibition and/or stimulation of various mitogen-activated protein kinase activities and inhibition of nuclear factor binding κB site (NF-κB) activation. Moreover, aspirin-like compounds have recently been shown to have previously unappreciated clinical and biological effects, some apparently independent of cyclooxygenase. In this review we discuss the various mechanisms of action of aspirin-like compounds and their relevance to clinical disease and therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000180050432
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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