Caffeic acid has antipromastigote activity by apoptosis-like process; and anti-amastigote by TNF-α/ROS/NO production and decreased of iron availability

Phytomedicine : International Journal of Phytotherapy and Phytopharmacology
Bruna Taciane da Silva BortoletiWander Rogério Pavanelli

Abstract

Leishmaniasis is a disease caused by protozoan parasites of the Leishmania genus whose current treatment has high cost, highly toxic, and difficult administration, which makes it very important to find alternative natural compounds of high efficiency and low cost. This study assessed the in vitro effect of caffeic acid (CA) on promastigotes and L. amazonensis-infected macrophages. Evaluation of the in vitro leishmanicidal activity of CA against promastigotes and L. amazonensis infected peritoneal macrophages, as well its microbicide mechanisms. CA 12.5-100 µg/ml were able to inhibit promastigotes proliferation at all tested periods. The IC50, 12.5 µg/ml, also altered promastigote cell morphology and cell volume accompanied by loss of mitochondrial integrity, increase in reactive oxygen species (ROS) production, phosphatidylserine exposure, and loss of plasma membrane integrity - characterizing the apoptosis-like process. Moreover, CA reduced the percentage of infected macrophages and the number of amastigotes per macrophages increasing TNF-α, ROS, NO and reducing IL-10 levels as well as iron availability. CA showed in vitro antipromastigote and antiamostigote by increasing oxidant and inflammatory response important to eliminat...Continue Reading

Citations

Dec 18, 2020·Frontiers in Chemistry·Luiza F O GervazoniElmo E Almeida-Amaral
Apr 10, 2019·European Journal of Pharmacology·Milena Menegazzo Miranda-SaplaWander Rogerio Pavanelli
Jul 1, 2021·Parasitology·Letícia NishiAna Lúcia Falavigna-Guilherme
Jul 4, 2021·Biochimie·Simone S C OliveiraPatrícia Severino
Aug 7, 2021·Journal of Biomolecular Structure & Dynamics·Kaio Maciel de Santiago-SilvaMarcelle de Lima Ferreira Bispo

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis