| Autor: |
Alves AB; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., da Silva Bortoleti BT; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil.; Carlos Chagas Institute (ICC-Fiocruz-Pr), Curitiba 81310-020, PR, Brazil., Tomiotto-Pellissier F; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil.; Carlos Chagas Institute (ICC-Fiocruz-Pr), Curitiba 81310-020, PR, Brazil., Ganaza AFM; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Gonçalves MD; Laboratory of Biotransformation and Phytochemistry, Department of Chemistry, Center of Exact Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Carloto ACM; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Rodrigues ACJ; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Silva TF; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Nakazato G; Department of Microbiology, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Kobayashi RKT; Department of Microbiology, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Lazarin-Bidóia D; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Miranda-Sapla MM; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Costa IN; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Pavanelli WR; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil., Conchon-Costa I; Laboratory of Immunoparasitology of Neglected Diseases and Cancer, Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, Londrina 86057-970, PR, Brazil. |
| Abstrakt: |
American tegumentary leishmaniasis, a zoonotic disease caused by the Leishmania genus, poses significant challenges in treatment, including administration difficulty, low efficacy, and parasite resistance. Novel compounds or associations offer alternative therapies, and natural products such as oregano essential oil (OEO), extracted from Origanum vulgare , have been extensively researched due to biological effects, including antibacterial, antifungal, and antiparasitic properties. Silver nanoparticles (AgNp), a nanomaterial with compelling antimicrobial and antiparasitic activity, have been shown to exhibit potent leishmanicidal properties. We evaluated the in vitro effect of OEO and AgNp-Bio association on L. amazonensis and the death mechanisms of the parasite involved. Our results demonstrated a synergistic antileishmanial effect of OEO + AgNp on promastigote forms and L. amazonensis -infected macrophages, which induced morphological and ultrastructural changes in promastigotes. Subsequently, we investigated the mechanisms underlying parasite death and showed an increase in NO, ROS, mitochondrial depolarization, accumulation of lipid-storage bodies, autophagic vacuoles, phosphatidylserine exposure, and damage to the plasma membrane. Moreover, the association resulted in a reduction in the percentage of infected cells and the number of amastigotes per macrophage. In conclusion, our findings establish that OEO + AgNp elicits a late apoptosis-like mechanism to combat promastigote forms and promotes ROS and NO production in infected macrophages to target intracellular amastigote forms. |
