摘要
The mast cell-mediated allergic reactions are involved in many allergic diseases, such as asthma, allergic rhinitis and sinusitis. Stimulation of mast cells initiates the process of degranulation, resulting in the release of mediators such as histamine and an array of inflammatory cytokines. In this report, we investigated the effect of gossypin (a biflavonoid) and suramin (a synthetic polysulphonated naphtylurea) on the mast cell-mediated allergy model, and studied the possible mechanism of their action. Both gossypin and suramin inhibited (P<0.001) compound 48/80-induced systemic anaphylaxis reactions, antiprurities (P<0.001) and reduced the histamine release in rats. Further, both showed significant (P<0.001) protection against rat peritoneal mast cells activated by compound 48/80. Thus, our findings provide evidence that gossypin and suramin inhibit mast cell-derived allergic reactions.
Subject(s)
Anaphylaxis/chemically induced , Anaphylaxis/drug therapy , Anaphylaxis/immunology , Animals , Anti-Allergic Agents/pharmacology , Anti-Allergic Agents/therapeutic use , Antipruritics/pharmacology , Antipruritics/therapeutic use , Ascitic Fluid/drug effects , Ascitic Fluid/metabolism , Bronchoalveolar Lavage Fluid , Disease Models, Animal , Flavonoids/pharmacology , Flavonoids/therapeutic use , Histamine Release/drug effects , Histamine Release/immunology , Hypersensitivity/blood , Hypersensitivity/drug therapy , Hypersensitivity/immunology , Hypersensitivity/metabolism , Mast Cells/drug effects , Mast Cells/immunology , Mast Cells/metabolism , Mice , Nitrogen Oxides/blood , Nitrogen Oxides/metabolism , Rats , Suramin/pharmacology , Suramin/therapeutic use , p-Methoxy-N-methylphenethylamine/pharmacology摘要
The antinociceptive effect of purine nucleotides administered systemically (sc) was determined using the formalin and writhing tests in adult male albino mice. The mechanisms underlying nucleotide-induced antinociception were investigated by preinjecting the animals (sc) with specific antagonists for opioid (naloxone, 1 mg/kg), purinergic P1 (caffeine, 5, 10 or 30 mg/kg); theophylline, 10 mg/kg) or purinergic P2 receptors (suramin, 100 mg/kg; Coomassie blue, 30-300 mg/kg; quinidine, 10 mg/kg). Adenosine, adenosine monophosphate (AMP), diphosphate (ADP) and triphosphate (ATP) caused a reduction in the number of writhes and in the time of licking the formalin-injected paw. Naloxone had no effect on adenosine- or adenine nucleotide-induced antinociception. Caffeine (30 mg/kg) and theophylline (10 mg/kg) reversed the antinociceptive action of adenosine and adenine nucleotide derivatives in both tests. P2 antagonists did not reverse adenine nucleotide-induced antinociception. These results suggest that the antinociceptive effect of adenine nucleotides is mediated by adenosine.