Inibição beta-adrenérgica reduz a incidência e o crescimento do carcinoma espinocelular de boca induzido por 4NQO em ratos

• Autor(a) principal: Cecilio, Heitor Pinhata [UNESP]
• Data de Publicação: 2017
• Tipo de documento: Trabalho de conclusão de curso
• Idioma: por
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://hdl.handle.net/11449/156654; http://www.athena.biblioteca.unesp.br/exlibris/bd/capelo/2018-06-12/000900826.pdf
• topic: Cancer; Neoplasias bucais; Carcinogênese; Receptores adrenérgicos; Propranolol; Mouth neoplasms

Recent studies have shown that beta-adrenergic receptors activation can influence cancer progression. However, there are no studies which have investigated the role of beta-adrenergic receptors on the oral carcinogenesis in preclinical models. The main goal of this study was to evaluate the effects of beta-adrenergic inhibition on the chemically induced oral carcinogenesis in rats. Sixty-four male Wistar rats were divided into two groups: Propranolol group: The animals were treated with a beta-adrenergic antagonist propranolol (10mg/kg diluted in PBS via subcutaneous); Control group (Sham): The animals were treated subcutaneously with vehicle alone (PBS). Both groups were submitted to an oral carcinogenesis model by the treatment with carcinogen 4-nitroquinoline-1-oxide (4NQO) diluted in drinking water for 16 weeks. After 16 weeks of carcinogenic induction, the animals were euthanized and the tongue was removed. Histopathological examination was performed to evaluate the presence and extention of tongue squamous cell carcinomas (SCCs). Specific statistical tests were performed to evaluate the differences in the cancer incidence and progression between the two experimental groups. Our results showed that rats in the Propranolol Group had a lower tumor incidence and thickness when compared to the control group. However, our tests did not show significant diferences between tumor volume and degree of malignacy when the groups were compared. Knowing that, the beta-adrenergic signaling blockade may reduce cancer incidence and thickness on a preclinical model