arthus reaction/protease

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Protease inhibitors reduce the reverse passive Arthus reaction.

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Trasylol, ovomucoid, tranexamic acid and soybean inhibitor decrease the vascular permeability as measured by extravasation of 131I-albumin when injected with the antibody at induction of a reverse passive Arthus reaction in the rat skin. Trasylol given systemically also had a suppressive effect,

FURTHER STUDY OF CORRELATIVE BEHAVIOR BETWEEN SPECIFIC PROTEASE AND ITS INHIBITOR IN CUTANEOUS ARTHUS REACTIONS.

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[On the increase in the serum protease activity (dipeptidase and tripeptidase) in the Arthus phenomenon].

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[Changes in the middle ear mucosa following administration of inflammatory proteases extracted from the regions with Arthus reaction].

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[On the significance of proteases for the Arthus reaction and pharmacologically induced edema in rat paws].

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The natural mediator for PMN emigration in inflammation. VI. Production of leucoegresin by inflammatory SH-dependent protease in active Arthus reactions in complement-depleted rabbits.

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The Arthus reaction in rodents: species-specific requirement of complement.

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We induced reverse passive Arthus (RPA) reactions in the skin of rodents and found that the contribution of complement to immune complex-mediated inflammation is species specific. Complement was found to be necessary in rats and guinea pigs but not in C57BL/6J mice. In rats, within 4 h after

NPC 15669 inhibits the reversed passive Arthus reaction in rats by blocking neutrophil recruitment.

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NPC 15669, N-carboxy-L-leucine,N-[(2,7-dimethylfluoren-9-yl)methyl]ester, has been shown to inhibit several inflammatory reactions that depend upon recruitment of neutrophils into the primary lesion. In the present study we examined the effects of NPC 15669 in the reversed passive Arthus reaction,

Role of thrombin and plasmin in development of delayed hypersensitivity reaction in guinea pig skin.

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Induration is a prominent feature of delayed hypersensitivity reaction (DHR), and fibrin deposition is the central mechanism. We studied the effects of two inhibitors of DHR on the activities of thrombin and plasmin in the extract of the skin site of DHR and compared the two activities in the site

Inhibition of various immunological reactions in vivo by a new synthetic complement inhibitor.

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FUT-175 (6 amidino-2-naphthyl-4-guanidino benzoate-dimethanesulfonate), a new synthetic protease inhibitor, inhibits the enzyme activities of various proteases, such as Clr, C1 esterase, thrombin, kallikrein, plasmin and trypsin. FUT-175 strongly inhibited complement-medicated hemolysis via the

The effect of FUT-175 (Nafamstat Mesilate) on C3a, C4a and C5a generation in vitro and inflammatory reactions in vivo.

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FUT-175 is a synthetic protease inhibitor and an inhibitor of the classical and alternate pathways of complement activation. In human serum, FUT-175 inhibited C3a, C4a and C5a generation induced by heat aggregated IgG, zymosan and Cobra venom factor with IC50 values in the range of 3-43 microM

[Pharmacological studies of FUT-175, nafamstat mesilate. III. Anti-inflammatory activities of FUT-175].

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Anti-inflammatory effects of FUT-175 (nafamstat mesilate), a new synthetic serine protease inhibitor, on various types of experimental inflammation were investigated in vivo and in vitro, in comparison with non-steroidal anti-inflammatory drugs (NSAID). The in vivo studies showed that FUT-175 has

Effects of all-trans retinoic acid on neutrophil-mediated endothelial cell injury in vitro and immune complex injury in rats.

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All-trans retinoic acid (RA) has beneficial effects when used in a variety of inflammatory skin conditions. In this study, the authors found that RA inhibited superoxide anion production and proteolytic enzyme release by human and rat neutrophils. Concomitantly, the authors found that RA-treated

Site of blood vessel damage and relevance of CD18 in a murine model of immune complex-mediated vasculitis.

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How neutrophils (polymorphonuclear neutrophils, PMNs) damage vessels in leukocytoclastic vasculitis (LcV) mediated by immune complexes (ICs) is unclear. If degradative enzymes and oxygen radicals are released from PMNs while adhering to the inner side of the vessel wall, they could be washed away by

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