TENIDAP, IN CONTRAST TO SEVERAL AVAILABLE NONSTEROIDAL ANTIINFLAMMATORY DRUGS, POTENTLY INHIBITS THE RELEASE OF ACTIVATED NEUTROPHIL COLLAGENASE

被引:34
作者
BLACKBURN, WD
LOOSE, LD
HECK, LW
CHATHAM, WW
机构
[1] VET ADM MED CTR,DIV CLIN IMMUNOL & RHEUMATOL,BIRMINGHAM,AL 35233
[2] UNIV ALABAMA,BIRMINGHAM,AL 35294
[3] PFIZER INC,DIV CENT RES,GROTON,CT 06340
来源
ARTHRITIS AND RHEUMATISM | 1991年 / 34卷 / 02期
关键词
D O I
10.1002/art.1780340213
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Neutrophils contain a collagenase that is stored in a latent form within the specific granule. With cellular activation, the latent enzyme is activated in association with the production of a variety of oxidants, including hypochlorous acid. We evaluated 4 nonsteroidal antiinflammatory drugs (NSAIDs) currently on the market and the new antiinflammatory/antirheumatic drug tenidap for their effects on the release of activated collagenase. In contrast to the 4 NSAIDs, tenidap profoundly inhibited the release of activated collagenase. This inhibition was predominantly due to interference with activation of the latent enzyme, rather than interference with enzyme release. The inhibition of collagenase activation was associated with a profound reduction in myeloperoxidase activity and in hypochlorous acid production. These observations demonstrate that tenidap has properties that set it apart from conventional NSAIDs and suggest that it may be a particularly useful agent in the treatment of inflammatory rheumatic disorders.
引用
收藏
页码:211 / 216
页数:6
相关论文
共 24 条
[1]   CHANGES IN THE VISCOSITY OF HYALURONIC-ACID AFTER EXPOSURE TO A MYELOPEROXIDASE-DERIVED OXIDANT [J].
BAKER, MS ;
GREEN, SP ;
LOWTHER, DA .
ARTHRITIS AND RHEUMATISM, 1989, 32 (04) :461-467
[2]   NEUTROPHIL ACTIVATION BY SURFACE BOUND IGG - PERTUSSIS TOXIN INSENSITIVE ACTIVATION [J].
BLACKBURN, WD ;
HECK, LW .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1988, 152 (01) :136-142
[3]   A LOW-MOLECULAR-WEIGHT, HEAT-LABILE FACTOR ENHANCES NEUTROPHIL FC RECEPTOR MEDIATED LYSOSOMAL-ENZYME RELEASE AND PHAGOCYTOSIS [J].
BLACKBURN, WD ;
HECK, LW ;
KOOPMAN, WJ ;
GRESHAM, HD .
ARTHRITIS AND RHEUMATISM, 1987, 30 (09) :1006-1014
[4]   INDUCTION OF NEUTROPHIL ENZYME-RELEASE BY RHEUMATOID FACTORS - EVIDENCE FOR DIFFERENCES BASED ON MOLECULAR CHARACTERISTICS [J].
BLACKBURN, WD ;
KOOPMAN, WJ ;
SCHROHENLOHER, RE ;
HECK, LW .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1986, 40 (02) :347-355
[5]   LIGAND-DEPENDENT RELEASE OF ACTIVE NEUTROPHIL COLLAGENASE [J].
CHATHAM, WW ;
HECK, LW ;
BLACKBURN, WD .
ARTHRITIS AND RHEUMATISM, 1990, 33 (02) :228-234
[6]   ANTIARTHRITIC DRUGS CONTAINING THIOL-GROUPS SCAVENGE HYPOCHLORITE AND INHIBIT ITS FORMATION BY MYELOPEROXIDASE FROM HUMAN-LEUKOCYTES - A THERAPEUTIC MECHANISM OF THESE DRUGS IN RHEUMATOID-ARTHRITIS [J].
CUPERUS, RA ;
MUIJSERS, AO ;
WEVER, R .
ARTHRITIS AND RHEUMATISM, 1985, 28 (11) :1228-1233
[7]  
DAVIS J S, 1988, Arthritis and Rheumatism, V31, pS72
[8]   EFFECT OF OXYGEN-DERIVED FREE-RADICALS ON HYALURONIC-ACID [J].
GREENWALD, RA ;
MOY, WW .
ARTHRITIS AND RHEUMATISM, 1980, 23 (04) :455-463
[9]  
HARRIS ED, 1980, COLLAGENASE NORMAL P
[10]  
HASTY KA, 1987, J BIOL CHEM, V262, P10048