Scholarship 23/05873-4 - Síndromes mielodisplásicas, Transdução de sinais - BV FAPESP
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Evaluation of signaling pathways, apoptosis and reactive oxygen species in an experimental model of myelodysplastic syndrome treated with artesunate

Grant number: 23/05873-4
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date until: June 01, 2023
End date until: May 31, 2024
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal Investigator:Sara Teresinha Olalla Saad
Grantee:João Vitor Facco
Host Institution: Centro de Hematologia e Hemoterapia (HEMOCENTRO). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated research grant:17/21801-2 - Predictors of severity and new treatments for bone marrow neoplasias, AP.TEM

Abstract

Artesunate is one of the semi-synthetic derivatives of artemisinin - active ingredient isolated from Artemisia annua L., a famous antimalarial. Recent studies show that this compound has anti-inflammatory, antileishmanial, immunomodulatory and antitumor effects. Our group showed that the treatment of transgenic mice presenting the fusion of the NUP98-HOXD13 genes, which develop Acute Myeloid Leukemia, led to modifications in cellular phenotypes, as well as alterations in more quiescent cells in the bone marrow, producing systemic antitumor effects, but which still need further investigation. The mice treatment with ART induced differences in the bone marrow of the mice. We found a decrease in the percentage of macrophages and neutrophils with an immunosuppressive phenotype, in addition to an increase in the production capacity of reactive oxygen species by monocytes. Furthermore, our data showed that ART treatment induced a significant increase in Natural Killer cells in the bone marrow microenvironment. Studies with artemisinin derivatives have shown that these compounds modulate several signaling pathways involved in the inflammatory process and apoptosis. Artemisinin derivatives also act on the NF-ºB signaling pathway. Furthermore, they can induce apoptosis by the generation of reactive oxygen species, along with the dynamic release of cytochrome c and the breakdown of different pro-caspases. Our data and the existing bibliography suggest important modulations induced by the compound, but which still require further studies.

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