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Título : Citral and eugenol modulate DNA damage and pro-inflammatory mediator genes in murine peritoneal macrophages.
Autor : Porto, Marília de Paula
Silva, Glenda Nicioli da
Luperini, Bruno Cesar Ottoboni
Pinelli, Tatiana Fernanda Bachiega
Marcondes, João Paulo de Castro
Sforcin, José Maurício
Salvadori, Daisy Maria Fávero
Palabras clave : Chemoprevention
Gene expression
Doxorubicin
Fecha de publicación : 2014
Citación : PORTO, M. de P. et al. Citral and eugenol modulate DNA damage and pro-inflammatory mediator genes in murine peritoneal macrophages. Molecular Biology Reports, v. 41, n. 11, p. 7043–7051, nov. 2014. Disponível em: <https://link.springer.com/article/10.1007%2Fs11033-014-3657-9>. Acesso em: 09 dez. 2019.
Resumen : Citral and eugenol have been broadly studied because of their anti-inflammatory, antioxidant and antiparasitic potentials. In this study, the effects of citral (25, 50 and 100 µg/mL) and eugenol (0.31, 0.62, 1.24 and 2.48 µg/mL) on the expression (RT-PCR) of the pro-inflammatory mediator genes NF-κB1, COX-2 and TNF-α were evaluated in mouse peritoneal macrophages with or without activation by a bacterial lipopolysaccharide (LPS). Additionally, the genotoxic potentials of two compounds and their capacities to modulate the DNA damage induced by doxorubicin (DXR) were investigated using the comet assay. The data revealed that neither citral nor eugenol changed COX-2, NF-κB1 or TNF-α expression in resting macrophages. However, in LPS-activated cells, citral induced the hypoexpression of COX-2 (100 µg/mL) and TNF-α (50 and 100 µg/mL). Hypoexpression of TNF-α was also detected after cellular exposure to eugenol at the highest concentration (2.48 µg/mL). Both compounds exhibited genotoxic potential (citral at 50 and 100 µg/mL and eugenol at all concentrations) but also showed chemopreventive effects, in various treatment protocols. Both citral and eugenol might modulate inflammatory processes and DXR-induced DNA damage, but the use of these compounds must be viewed with caution because they are also able to induce primary DNA lesions.
URI : http://www.repositorio.ufop.br/handle/123456789/11850
metadata.dc.identifier.uri2: https://link.springer.com/article/10.1007%2Fs11033-014-3657-9
metadata.dc.identifier.doi: https://doi.org/10.1007/s11033-014-3657-9
ISSN : 1573-4978
Aparece en las colecciones: DEACL - Artigos publicados em periódicos

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