Use este identificador para citar ou linkar para este item: http://www.repositorio.ufop.br/jspui/handle/123456789/4744
Título: Naringin accelerates the regression of pre-neoplastic lesions and the colorectal structural reorganization in a murine model of chemical carcinogenesis.
Autor(es): Sequetto, Priscila Lima
Oliveira, Tânia Toledo de
Maldonado, Izabel Regina dos Santos Costa
Augusto, Luís Eugênio Franklin
Mello, Vanessa Joia de
Pizziolo, Virgínia Ramos
Almeida, Márcia Rogéria de
Silva, Marcelo Eustáquio
Novaes, Rômulo Dias
Palavras-chave: Flavonoide
Large intestine
Pathology
Toxicology
Data do documento: 2014
Referência: SEQUETTO, P. L. et al. Naringin accelerates the regression of pre-neoplastic lesions and the colorectal structural reorganization in a murine model of chemical carcinogenesis. Food and Chemical Toxicology, v. 64, p. 200-209, 2014. Disponível em: <http://www.sciencedirect.com/science/article/pii/S0278691513007941>. Acesso em: 20 fev. 2015.
Resumo: The aim of this study was to investigate the effect of Naringin on pre-neoplastic colorectal lesions induced by chemical carcinogen in rats. Female Wistar rats weighing 130.8 ± 27.1 g received weekly one subcutaneous injection of 1,2-dimethylhydrazine (DMH, 20 mg/kg) for 10 weeks. The animals were divided into 5 groups with 6 animals in each group. Group 1: 0.9% saline; Group 2: DMH + 0.9% saline; Group 3: DMH + Naringin (10 mg/kg); Group 4: DMH + Naringin (100 mg/kg); Group 5: DMH + Naringin (200 mg/kg). G2 and G3 showed a significant increase in ACF number, AgNOR/nucleus and mitosis compared to G1. G4 and G5 presented a significant reduction in these parameters compared to G2. The number of cells producing acidic and neutral mucins, red blood cells and the level of antioxidant minerals, such as copper, magnesium, selenium and zinc, were significantly reduced in G2 and G3, but similar in G4 and G5 compared to G1. Naringin, especially at 200 mg/kg, was effective in reducing the number of pre-neoplastic lesions in rats exposed to DMH. Some of these effects may be due to reduction in cellular proliferation and tissue levels of iron together with the recovery of antioxidant mineral levels induced by this flavonoid.
URI: http://www.repositorio.ufop.br/handle/123456789/4744
DOI: https://doi.org/10.1016/j.fct.2013.11.032
ISSN: 0278-6915
Licença: O periódico Food and Chemical Toxicology concede permissão para depósito deste artigo no Repositório Institucional da UFOP. Número da licença: 3574840745128.
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