Navegando por Palavras-chave "anti-inflammatory agents"

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    Antinociceptive effect of purine nucleotides
    (Assoc Bras Divulg Cientifica, 1996-10-01) Mello, C. F.; Begnini, J.; DeLaVega, D. D.; Lopes, F. P.; Schwartz, C. C.; JimenezBernal, R. E.; Bellot, Rogerio Gentil [UNIFESP]; Frussa-Filho, Roberto [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    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 P-1 (caffeine, 5, 10 or 30 mg/kg); theophylline, 10 mg/kg) or purinergic P-2 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. P-2 antagonists did not reverse adenine nucleotide-induced antinociception. These results suggest that the antinociceptive effect of adenine nucleotides is mediated by adenosine.
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    Effect of anti-inflammatory agents on the integration of autogenous bone graft and bovine bone devitalized matrix in rats
    (Acta Cirurgica Brasileira, 2008-03-01) Silva, Roberto Antoniolli da [UNIFESP]; Fagundes, Djalma José [UNIFESP]; Silva, Andreia Conceicao Milan Brochado Antoniolli; Sisti, Karin Ellen; Carvalho, Themis Maria Milan Brochado de; Silva, Daniel Nunes e; Universidade Federal de Mato Grosso do Sul (UFMS); Universidade Federal de São Paulo (UNIFESP)
    Purpose: To study the repair of bone defect filled with autograft or bovine bone devitalized matrix in rats under anti-inflammatory action. Methods: Two hundred and forty Wistar rats were distributed to two groups of 120 animals each. A 2mm-diameter defect was created in the femoral diaphysis. Animals of Group I had the bone defect filled with autograft and those of Group II, with bovine bone devitalized matrix. Animals of each group were redistributed to four subgroups according to the intramuscular administration of anti-inflammatory drug or saline solution: A - diclofenac sodium; B - dexamethasone; C - meloxicam; D - saline solution. Evaluation periods were 7, 14 and 30 days. Histological evaluation consisted of quantifying the inflammatory process, the bone neoformation, the collagen formation and the presence of macrophages. Results: Animals of Group I did not show significant difference considering inflammatory reaction. Significant and progressive increase of bone neoformation was observed in both groups. The animals that received meloxicam and autograft showed less collagen formation at 14 and 30 days. The number of macrophages was higher in Group II than in Group I. The animals treated with dexamethasone and saline Solution did not show statistically significant difference. Conclusions: Diclofenac sodium and meloxicam delayed bone graft repair and dexamethasone did not interfere in it.
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    Long-lasting neuroprotective effect of postischemic hypothermia and treatment with an anti-inflammatory/antipyretic drug - Evidence for chronic encephalopathic processes following ischemia
    (Amer Heart Assoc, 1996-09-01) Coimbra, Cicero [UNIFESP]; Drake, M.; BorisMoller, F.; Wieloch, T.; LUND UNIV; Universidade Federal de São Paulo (UNIFESP)
    Background and Purpose It has been recognized that post ischemic pharmacological interventions may delay the evolution of neuronal damage rather than provide long-lasting neuroprotection. Also, fever complicates recovery after stroke in humans. Here we report the effects of late postischemic treatment with hypothermia and an antipyretic/anti-inflammatory drug, dipyrone, on cell damage at 1 week and 2 months of survival.Methods Rats were subjected to 10 minutes of forebrain ischemia. Hypothermia (33 degrees C) was induced at 2 hours of recovery and maintained for 7 hours. Dipyrone (100 mg . kg(-1)IP) was given every 3 hours from 14 to 72 hours of recovery. Temperature was measured every 6 hours for 60 days. Neuronal damage was assessed at 7 days and 2 months of recovery.Results From 17 to 72 hours of recovery, a period of hyperthermia was observed, which dipyrone abolished but postischemic hypothermia treatment did not. Dipyrone treatment diminished neuronal damage by 43% at 7 days, and at 2 months of survival, a minor (168) protection was seen. Postischemic hypothermia treatment alone delayed neuronal damage. In contrast, combined treatment of hypothermia followed by dipyrone markedly diminished neuronal damage by more than 50% at both 7 days and 2 months of recovery.Conclusions Neuronal degeneration may be ongoing for months after a transient ischemic insult, and prolonged protective measures need to be instituted for long-lasting neuroprotective effects. Hyperthermia during recovery worsens ischemic damage, and processes associated with inflammation may contribute to the development of neuronal damage. An early and extended period of postischemic hypothermia provides a powerful and long-lasting protection if followed by treatment with anti-inflammatory/antipyretic drugs.