RESUMO
AIMS: To develop a behavioral model in mice that is capable of mimicking some distinctive symptoms of human posttraumatic trigeminal neuropathic pain such as spontaneous pain, cold allodynia, and chemical÷inflammatory hyperalgesia, and to use this model to investigate the antinociceptive effects of clomipramine and tramadol, two drugs used for the treatment of neuropathic pain. METHODS: A partial tight ligature of the right infraorbital nerve by an intraoral access or a sham procedure was performed. Fourteen days later, mice were subcutaneously injected with saline or drugs and the spontaneous nociceptive behavior, as well as the responses to topical acetone and to formalin or capsaicin injected into the ipsilateral vibrissal pad, were assessed. Data were analyzed by ANOVA. RESULTS: Neuropathic mice exhibited an increased spontaneous rubbing÷scratching of the ipsilateral vibrissal pad, together with enhanced responses to cooling (acetone) and the chemical irritants (formalin, capsaicin). Clomipramine and tramadol produced an antihyperalgesic effect on most of these nociceptive responses, but tramadol was ineffective on capsaicin-induced hyperalgesia. CONCLUSION: Nociceptive responses in this neuropathic pain model in mice exhibited a pattern consistent with the pain described by posttraumatic trigeminal neuropathic patients. The selective antihyperalgesic effect obtained with two commonly used drugs for treating neuropathic pain confirms the validity of this preclinical model.
Assuntos
Analgésicos Opioides/uso terapêutico , Clomipramina/uso terapêutico , Hiperalgesia/tratamento farmacológico , Inibidores Seletivos de Recaptação de Serotonina/uso terapêutico , Tramadol/uso terapêutico , Traumatismos do Nervo Trigêmeo/complicações , Neuralgia do Trigêmeo/tratamento farmacológico , Acetona/efeitos adversos , Animais , Capsaicina/efeitos adversos , Modelos Animais de Doenças , Formaldeído/efeitos adversos , Irritantes/efeitos adversos , Masculino , Camundongos , Nociceptores/efeitos dos fármacos , Órbita/inervação , Prurido/etiologia , Fármacos do Sistema Sensorial/efeitos adversos , Canal de Cátion TRPA1 , Canais de Cátion TRPV/efeitos dos fármacos , Canais de Potencial de Receptor Transitório/efeitos dos fármacos , Neuralgia do Trigêmeo/etiologia , Vibrissas/efeitos dos fármacos , Vibrissas/inervaçãoRESUMO
OBJECTIVE: As resin-modified glass-ionomer cement (RMGIC) is an adhesive material, its association to dentin bonding agents (DBAs) was previously proposed. This study investigated the adjunctive behavior of an RMGIC with etch-and-rinse bonding systems under in situ/ex vivo cariogenic challenge. METHOD AND MATERIALS: Bovine enamel blocks (3 3 3 3 2 mm) were randomly assigned to group VP, Vitremer + its own primer (3M ESPE); group VSB, Vitremer + Single Bond (3M ESPE); and group VPB, Vitremer + Prime and Bond 2.1 (Dentsply). Two blocks of each group were randomly placed in an acrylic palatal appliance, so each appliance included six blocks. Volunteers (n = 10) wore these appliances according to given instructions to promote a sucrose challenge eight times/day for 15 days. After this period, the blocks were removed from the devices and cleaned, and demineralization was assessed through longitudinal microhardness analysis (Knoop indenter, 25 g/5 s). Data were submitted to three-way ANOVA and Tukey test (P < .05). RESULTS: No treatment was able to completely avoid demineralization. All materials showed a statistically significant difference in mineral loss when the microhardness on the outer enamel was compared with deeper regions (P < .05). CONCLUSION: Association of the tested RMGICs with etch-and-rinse DBAs did not seem to be more beneficial against caries than the conventional treatment with RMGIC.
Assuntos
Cariostáticos/uso terapêutico , Adesivos Dentinários/efeitos adversos , Cimentos de Ionômeros de Vidro/uso terapêutico , Cimentos de Resina/efeitos adversos , Desmineralização do Dente/prevenção & controle , Acetona/efeitos adversos , Análise de Variância , Animais , Bis-Fenol A-Glicidil Metacrilato/efeitos adversos , Bovinos , Resinas Compostas/uso terapêutico , Estudos Transversais , Esmalte Dentário , Interações Medicamentosas , Cimentos de Ionômeros de Vidro/química , Dureza , Humanos , Ácidos Polimetacrílicos/efeitos adversos , Estatísticas não ParamétricasRESUMO
PURPOSE: To evaluate the antitumor effect of acetone cyanohydrin in Ehrlich ascites tumor cells in vitro. METHODS: The Ehrlich ascites tumor cells and lymphocytes were incubated with different concentrations of acetone cyanohydrin (0, 0.5, 1.0, 2.0, 10.0, 20.0 and 30.0 μg.mL-1), After 1, 2, 3, 4, 18 and 24 hours cell viability tests were performed by the trypan blue method. RESULTS: The results demonstrated a dose-dependent cytotoxic effect against the cells of Ehrlich ascites tumor. The concentrations of 20 and 30 μg.mL-1 was 100 percent of cell death in only 1 and 2 hours respectively. In lower doses of 0.5, 1.0 and 2.0 μg.mL-1 the cytotoxic effect was less intense, increasing gradually with time. CONCLUSIONS: At low concentrations of 0.5, 1.0 and 2.0 μg.mL-1, more than 90 percent of cell death was observed only after 24 hours of incubation which is the evidence that the tumor cell has the ability to poison cumulatively and irreversibly itself with the acetone cyanohydrin when compared with the results presented by human lymphocytes that the same doses and at the same time of incubation reached a maximum of 30 percent of cell death, suggesting an activity of rhodanese differentiated between the two cells.(AU)
OBJETIVO: Avaliar o efeito antitumoral da acetona cinidrina em células do tumor ascítico de Ehrlich in vitro. MÉTODOS: Células do tumor ascítico de Ehrlich e linfócitos foram incubadas com diferentes concentrações de acetona cianidrina (0, 0,5, 1,0, 2,0, 10,0, 20,0 e 30,0 μg.mL-1), depois de 1, 2, 3, 4, 18 e 24 horas foi verificada a viabilidade celular atravéz do método de azul de trypan. RESULTADOS: Os resultados demonstraram um efeito citotóxico dose dependente frente as células do tumor ascítico de Ehrlich. Nas concentrações de 20 e 30 μg.mL-1 ocorreu 100 por cento de morte celular em apenas 1 e 2 horas respectivamente. Nas doses mais baixas de 0,5, 1,0 e 2,0 μg.mL-1 o efeito citotóxico foi menos intenso, aumentando gradativamente com o tempo. CONCLUSÕES: Nas concentrações baixas de 0,5. 1,0 e 2,0 μg.mL-1, foi observado mais de 90 por cento de morte celular somente após 24 horas de incubação o que evidência a capacidade da célula tumoral de se intoxicar de maneira irreversível e acumulativa com a acetona cianidrina, quando comparadas com os resultados apresentados pelos linfócitos humanos que nas mesmas doses e nos mesmos tempos de incubação atingiram um máximo de 30 por cento de morte celular, o que sugere uma atividade de rodanase diferenciada entre as duas células.(AU)
Assuntos
Animais , Masculino , Ratos , Acetona/efeitos adversos , Carcinoma de Ehrlich/tratamento farmacológico , Citotoxinas/administração & dosagem , Citotoxinas/efeitos adversos , Acetona/administração & dosagem , Neoplasias/tratamento farmacológicoRESUMO
Con el objetivo de precisar las alteraciones morfológicas producidas por la aplicación de un condensado de humo de cigarrillos sobre la mucosa labial y su relación con el tiempo de aplicación del carcinógeno, se seleccionaron 120 ratones IBFI entre 4 y 6 semanas de nacido. Los animales recibieron alimento y agua ad libitum y fueron divididos en 4 grupos. Dos grupos fueron tratados con carcinógenos, unos de ellos con el benzo (a) pireno y el otro con un condensado de humo de cigarrillos negros. Un tercer grupo fue tratado con acetona y quedó un grupo no tratado como control. Durante 44 semanas se aplicaron 10 *L de las sustancias empleadas en la mucosa labial de los animales 3 veces a la semana. Todos los animales fueron autopsiados y se realizó disección de labio y lengua. En la semana 44 se presentaron carcinoma epidermoides evidentes tanto en los grupos que recibieron benzo (a) pireno como condensado de humo. Las modificaciones hísticas, más relevantes en diferentes etapas fueron la queratinización superficial, el grosor epitelial y la displasia previas a los estadios neoplásticos