Asunto(s)
Enfermedades de los Genitales Masculinos/patología , Histiocitosis Sinusal/patología , Escroto/patología , Piel/patología , Biomarcadores/análisis , Biopsia , Enfermedades de los Genitales Masculinos/inmunología , Enfermedades de los Genitales Masculinos/metabolismo , Enfermedades de los Genitales Masculinos/cirugía , Histiocitosis Sinusal/inmunología , Histiocitosis Sinusal/metabolismo , Histiocitosis Sinusal/cirugía , Humanos , Inmunohistoquímica , Lactante , Masculino , Escroto/química , Escroto/inmunología , Escroto/cirugía , Piel/química , Piel/inmunologíaRESUMEN
Rosmarinus officinalis L. (Lamiaceae), popularly known as rosemary, is used for food flavoring and in folk medicine as an antispasmodic, analgesic, antirheumatic, diuretic, and antiepileptic agent. Few studies have shown the anti-inflammatory effects of rosemary essential oil (REO). This study evaluated the effects of REO on leukocyte migration through in vivo leukocyte migration and in vitro chemotaxis assay. REO was analyzed by using gas chromatography-mass spectometry, and the main components identified were camphor (27.59%), 1,8-cineole (15.74%), α-pinene (16.58%), and ß-myrcene (10.02%). In rats, administration of REO reduced the number of leukocytes that rolled, adhered, and migrated to the scrotal chamber after carrageenan injection. All doses of REO tested significantly inhibited leukocyte chemotaxis induced by casein. The effects of REO on leukocyte migration highlight an important mechanism of the anti-inflammatory action of rosemary.
Asunto(s)
Antiinflamatorios no Esteroideos/farmacología , Inhibición de Migración Celular , Quimiotaxis de Leucocito/efectos de los fármacos , Leucocitos/efectos de los fármacos , Aceites Volátiles/farmacología , Animales , Antiinflamatorios no Esteroideos/administración & dosificación , Antiinflamatorios no Esteroideos/química , Carragenina/toxicidad , Ensayos de Migración de Leucocitos , Relación Dosis-Respuesta a Droga , Endotelio/citología , Endotelio/efectos de los fármacos , Endotelio/inmunología , Cromatografía de Gases y Espectrometría de Masas , Prueba de Inhibición de Adhesión Leucocitaria , Leucocitos/citología , Leucocitos/inmunología , Espectroscopía de Resonancia Magnética , Masculino , Medicina Tradicional , Monoterpenos/análisis , Monoterpenos/química , Monoterpenos/farmacología , Aceites Volátiles/administración & dosificación , Aceites Volátiles/química , Hojas de la Planta/química , Ratas , Ratas Wistar , Rosmarinus/química , Escroto/citología , Escroto/efectos de los fármacos , Escroto/inmunologíaRESUMEN
We investigated morphological alterations induced by s.c. injection of 2.5 microg of Bothrops jararaca venom in rats. Intense disorganisation of collagen fibres was observed 1 min after the venom injection, particularly at regions near vessels and nerves. Mast cells were degranulated, and erythrocytes were seen leaving venules throughout the endothelial junctions. At this time, damaged endothelial cells were not observed. In rats envenomed as above, but immediately after cardiorespiratory failure induced by deep ether anaesthesia, alterations in the connective tissue structures, as previously described, were not observed. The mediation of this haemorrhage was investigated by injecting the venom into the foot pad of mice and compared to the mediation of oedema. Local haemorrhage was significantly reduced in mice pre-treated with capsaicin or guanethidine or submitted to a surgical section of sciatic and saphenous nerves. In these animals, oedema was not affected. Groups treated with methysergide or morphine showed both haemorrhage and oedema significantly reduced. Indomethacin or dexamethasone pre-treatments significantly reduced the oedema, but not the haemorrhage. Moreover, in animals treated with promethazine or mepyramine, oedema and haemorrhage were not affected. These data suggest that local haemorrhage induced by Bothrops jararaca venom is partially controlled by serotonin and neurohumoral mediators. Furthermore, results indicate that haemorrhage and oedema are mediated by different pharmacological systems.