An in vitro mouse macrophage model for use in assessing the effects of anti-inflammatory drugs
Mononuclear phagocytic cells are implicated in many chronic inflammatory diseases1. In rheumatoid arthritis these cells, stimulated by inflammatory products, engulf immune complexes accumulating in the diseased joint, accompanied by a selective secretion of lysosomal acid hydrolases2. These have the capacity to activate complement and kinin pathways as well as inducing the destruction of the proteoglycan matrix of the joint3. Inhibition of the release of these hydrolases by lysosomal membrane stabilizing drugs may be an important means of reducing joint destruction in chronic arthritis3. Many anti-inflammatory drugs, e.g. hydrocortisone, dexamethasone, phenylbutazone and flufenamic acid, have been reported to stabilize lysosomal membranes4–6. With some of these compounds a correlation has been demonstrated between lysosomal stabilization effects in vitro and their antiinflammatory activities in vivo in animal models4.
KeywordsLysosomal Enzyme Enzyme Release Flufenamic Acid Lysosomal Enzyme Activity Zymosan Particle
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