Avaliação da atividade antileucêmica de extratos de fungos endofíticos
Ano de defesa: | 2018 |
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Autor(a) principal: | |
Orientador(a): | |
Banca de defesa: | |
Tipo de documento: | Dissertação |
Tipo de acesso: | Acesso aberto |
Idioma: | por |
Instituição de defesa: |
Universidade Federal de Mato Grosso
Brasil Faculdade de Medicina (FM) UFMT CUC - Cuiabá Programa de Pós-Graduação em Ciências da Saúde |
Programa de Pós-Graduação: |
Não Informado pela instituição
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Departamento: |
Não Informado pela instituição
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País: |
Não Informado pela instituição
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Palavras-chave em Português: | |
Link de acesso: | http://ri.ufmt.br/handle/1/3051 |
Resumo: | Despite advances in the treatment of leukemias, the chemotherapeutic agents available at the oncology clinic still show significant toxicity and high non-specificity. Therefore, the discovery of new sources of bioactive molecules for the treatment of leukemia is an important strategy for curing the disease. In this work, cytotoxicity and mechanism of cell death of endophytic fungi found in Axonopus leptostachyus were made in vitro. The extracts were obtained by maceration of the mycelium of the fungus with ethyl acetate and diluted in RPMI medium at the concentration of 100 μg / mL for cytotoxic assay. Were used 106 cells / mL of the Kasumi-1 leukemia lines (acute myeloid leukemia, ATCC® CCL-2724 ™), K562 (chronic myeloid leukemia, ATCC® CCL-243 ™) and Jurkat (acute lymphoblastic leukemia, ATCC® TIB-152 ™) in 96-well microplates incubated with extracts or vehicles in a 5% CO2 at 37 ° C for 24 hours. Cell viability was determined by the measure of propidium iodide fluorescence (620nm) by flow cytometry. Then, the most cytotoxic extracts were tested for IC 50, apoptosis, cell cycle analysis and membrane potential. At the end of the analyzes, extracts of Trichoderma strigosellum and Gibberella moniliformis demonstrated greater cytotoxic selectivity for the leukemic lines. The extract of T. strigosellum demonstrated to cause death by apoptosis and extract of G. moniliformis death by increase of reactive oxygen species without induction of apoptosis. |