Inhibition of Hepatocarcinogenesis by ArtinM via Anti-proliferative and Pro-apoptotic Mechanisms

Autor(es)

Braz, Mariana M. ; Roque-Barreira, Maria Cristina ; Ramalho, Fernando S. ; Oliveira, Carlos A. ; Augusto, Marlei J. ; Ramalho, Leandra N. Z.

• Tipo de documento: Artigo Científico
• Fonte: IN VIVO; v. 30, n. 6, p. 845-852, NOV-DEC 2016.
• Citações Web of Science: 1

Resumo

ArtinM is a d-mannose-binding lectin found in the seeds of Artocarpus heterophyllus (jackfruit) that interacts with N-glycans, that is associated with receptors on the surface of phagocytic cells and induces the production of inflammatory mediators. Some of them are especially important because they may be required for antitumor immune response. This study aimed to evaluate the effect of ArtinM on hepatocellular preneoplastic foci. Wistar rats received 50 mg/kg of diethyl-nitrosamine (DEN) intraperitoneal weekly for 12 weeks. From the 14th week, the treated animals received 50 mu g/kg of ArtinM subcutaneous every 2 weeks until the 18th week, whereas control animals were injected with vehicle alone. Preneoplastic-related factors were estimated using histological, western blotting and RT-PCR analysis. In comparison to the groups exposed to DEN, the ArtinM-treated rats showed diminution of preneoplastic foci, decreased expression of proliferating cell nuclear antigen (PCNA), increased number of nuclear p21 and p27 stained cells, augmented number of apoptotic cells, increased expression of p53, p42/44 MAPK and p21 proteins, reduced cyclin D1 (CCND1) protein levels and increased expression of TNF alpha and IFN gamma genes. No difference was observed in interleukin 12 (IL12) protein levels. These findings indicate that ArtinM may provide protection against hepatocarcinogenesis as a result of the induction of cell-cycle blockage and pro-apoptotic mechanisms. (AU)

• Processo FAPESP: 10/20895-4 - Avaliação de adutos AFB1-Lisina e AFB1-N7-guanina como biomarcadores de exposição humana e animal às aflatoxinas
• Beneficiário: Carlos Augusto Fernandes de Oliveira
• Modalidade de apoio: Auxílio à Pesquisa - Temático