beta-ionone inhibits nonalcoholic fatty liver disease and its association with hepatocarcinogenesis in male Wistar rats

Autor(es)

Paulino Miranda, Mayara Lilian ^[1] ; Furtado, Kelly Silva ^[1] ; Andrade, Fabia de Oliveira ^[1] ; Heidor, Renato ^[1] ; da Cruz, Raquel Santana ^[2] ; Nogueira, Marina Sayuri ^[3] ; de Castro, Inar Alves ^[3] ; Purgatto, Eduardo ^[4] ; Barbisan, Luis Fernando ^[5] ; Moreno, Fernando Salvador ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Fac Pharmaceut Sci, Dept Food & Expt Nutr, Lab Diet Nutr & Canc, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Fac Pharmaceut Sci, Dept Food & Expt Nutr, Lab Nutrigen & Programming Canc, Sao Paulo - Brazil

^[3] Univ Sao Paulo, Fac Pharmaceut Sci, Dept Food & Expt Nutr, Lab Dev Funct Foods, Sao Paulo - Brazil

^[4] Univ Sao Paulo, Fac Pharmaceut Sci, Dept Food & Expt Nutr, Lab Food Chem & Biochem, Sao Paulo - Brazil

^[5] Sao Paulo State Univ UNESP, Biosci Inst Botucatu, Dept Morphol, Lab Expt & Chem Carcinogenesis, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Chemico-Biological Interactions; v. 308, p. 377-384, AUG 1 2019.
• Citações Web of Science: 0

Resumo

Among the primary neoplasias that affect the liver, hepatocellular carcinoma (HCC) is the most frequent and the third leading cause of death related to cancer. Several risk factors predispose individuals to HCC such as nonalcoholic fatty liver disease (NAFLD), whose incidence has significantly increased worldwide. beta-ionone (beta I) isoprenoid is a known chemopreventive of hepatocarcinogenesis. However, the effects of this compound on NAFLD isolated or in association with hepatocarcinogenesis have not yet been evaluated. A high-fat emulsion administered for 6 weeks resulted in NAFLD in male rats, and oral treatment with beta I during this period significantly attenuated its development. Moreover, the presence of NAFLD potentiated hepatocarcinogenesis induced by the resistant hepatocyte (RH) model in these animals by increasing the number and percentage of the liver section area occupied by placental glutathione S-transferase (GST-P)-positive persistent preneoplastic lesions (pPNLs), that are thought to evolve into HCC. This indicates that this NAFLD/RH protocol is suitable for studies of the influence of NAFLD on the HCC development. Therefore, here we also investigated the chemopreventive effect of beta I under these two associated conditions. In this context, beta I reduced the number and percentage of the liver section area occupied by pPNLs, as well as cell proliferation and the number of oval cells, which are considered potential targets for the development of HCC. Thus, beta I presents not only a promising inhibitory effect on NAFLD isolated but also chemopreventive activity when it is associated with hepatocarcinogenesis. (AU)

• Processo FAPESP: 13/07914-8 - FoRC - Centro de Pesquisa em Alimentos
• Beneficiário: Bernadette Dora Gombossy de Melo Franco
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs