RESUMEN
AIM: To assess different concentrations and formulations of topical ozenoxacin using a mouse model of Staphylococcus aureus dermal infection for identification of the best formulation for treating patients with impetigo. MATERIALS & METHODS: The efficacy of ozenoxacin formulations was compared with vehicle control, mupirocin and retapamulin ointments in a mouse model. RESULTS: The most effective concentrations of ozenoxacin for reducing S. aureus counts after dermal application were 1 and 2%. Direct comparison of two batches of 1% ozenoxacin ointment and cream with 1% retapamulin and 2% mupirocin ointments in the mouse model showed superior efficacy of ozenoxacin. CONCLUSION: 1% ozenoxacin ointment and cream were the most effective formulations in significantly reducing bacterial load in S. aureus dermally infected mice.
Asunto(s)
Aminopiridinas/administración & dosificación , Antibacterianos/administración & dosificación , Impétigo/tratamiento farmacológico , Quinolonas/administración & dosificación , Staphylococcus aureus/efectos de los fármacos , Infección de Heridas/tratamiento farmacológico , Administración Tópica , Aminopiridinas/farmacología , Aminopiridinas/uso terapéutico , Animales , Animales no Consanguíneos , Antibacterianos/farmacología , Antibacterianos/uso terapéutico , Compuestos Bicíclicos Heterocíclicos con Puentes/administración & dosificación , Compuestos Bicíclicos Heterocíclicos con Puentes/farmacología , Compuestos Bicíclicos Heterocíclicos con Puentes/uso terapéutico , Modelos Animales de Enfermedad , Diterpenos , Relación Dosis-Respuesta a Droga , Humanos , Ratones , Mupirocina/administración & dosificación , Mupirocina/farmacología , Mupirocina/uso terapéutico , Pomadas , Quinolonas/farmacología , Quinolonas/uso terapéutico , Crema para la Piel/administración & dosificación , Crema para la Piel/farmacología , Crema para la Piel/uso terapéutico , Resultado del TratamientoRESUMEN
Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit prostaglandin synthesis in the gastrointestinal mucosa, which can lead not only to stomach ulcers but also ulcers in the small and large intestines. Ulcers of the small intestine are less common than those of the stomach, but intestinal lesions are more life threatening. Although the R(-)-enantiomers of the arylpropionic acid (APA) class of NSAIDs are assumed to lack the toxic effects of cyclooxygenase inhibition, they may contribute to the ulcerogenicity of racemates. We have examined the intestinal ulcerogenic effects of single oral doses of S(+)-ketoprofen compared with racemic ketoprofen in the small intestine and cecum of rats. The toxicity in the small intestine was measured as the weight ratio between portions of intestine showing lesions and the total weight of the tissue. Toxicity in the cecum was evaluated by measuring the size of the ulcers. S(+)-ketoprofen had no significant ulcerogenic effect at 10 or 20 mg/kg. However, racemic ketoprofen was clearly ulcerogenic in the small intestine and cecum at the 40 mg dose. R(-)-ketoprofen at 20 mg/kg does not show any effect in the cecum and only limited ulcerogenesis in the small intestine: The latter effect may be the result of racemic inversion. Therefore, the ulcerogenic action of racemic ketoprofen can be interpreted as a synergism between S(+)- and R(-)-ketoprofen. The mechanism of this synergism is not well understood but may be a general feature of APA NSAIDs.
