Evaluation of Rhinella marina Extracts on the Effector Functions of Human Neutrophils.
6 affiliations
- 1Postgraduate Program in Biotechnology and Biodiversity of the Pró Centro-Oeste Network, Federal University of Mato Grosso, Sinop 78557-267, MT, Brazil.
- 2Institute of Health Sciences, Federal University of Mato Grosso, Sinop 78557-267, MT, Brazil.
- 3Department of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto 14040-903, SP, Brazil.
- 4Postgraduate Program in Ecology and Biodiversity Conservation, Federal University of Mato Grosso, Cuiabá 78060-900, MT, Brazil.
- 5Secretariat of Science, Technology and Innovation of the State of Mato Grosso, Cuiabá 78020-450, MT, Brazil.
- 6Postgraduate Program in Chemistry, Federal University of Mato Grosso, Cuiabá 78060-900, MT, Brazil.
Abstract
Neutrophils play a central role in the innate immune response. However, in inflammatory and autoimmune diseases, the exacerbated activation of these cells can result in excessive release of reactive oxygen species (ROS), proteases, and inflammatory mediators, contributing to tissue damage. In this context, natural compounds derived from amphibian venoms have attracted interest due to their pharmacological and immunomodulatory potential. This study aimed to evaluate in vitro the effects of the crude methanolic extract (CME) of Rhinella marina on the effector functions of human neutrophils. For this purpose, peripheral blood neutrophils from healthy individuals were treated with CME (0.5, 5, and 50 µg/mL) or untreated controls. Cytotoxicity, total ROS production, superoxide anion production, myeloperoxidase (MPO) activity, elastase degranulation, NET (Neutrophil Extracellular Trap) formation, and parameters related to cellular redox status, including antioxidant enzymes and markers of oxidative damage, were evaluated. CME showed concentration-dependent cytotoxicity. There were no changes in ROS production by luminol-dependent chemiluminescence after stimulation with myristoylphorbol acetate (PMA). However, it reduced superoxide anion production in neutrophils in both stimuli in the NBT assay. CME did not significantly modulate MPO activity or NET formation, but it reduced elastase release, suggesting modulation of neutrophil degranulation. Additionally, it increased glutathione-S-transferase (GST) activity and reduced glutathione (GSH) levels. It can be concluded that CME partially modulated neutrophil effector functions, such as superoxide anion production and degranulation, in addition to exhibiting partial protective effects on cellular redox state parameters. These findings suggest the extract's immunomodulatory potential and reinforce the need for further studies to clarify its mechanisms of action and possible applicability in neutrophil-mediated inflammatory conditions.
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BibTeX
@article{albiero2026evaluation,
title = {{Evaluation of Rhinella marina Extracts on the Effector Functions of Human Neutrophils.}},
author = {Lucinéia Reuse Albiero and Valfran da Silva Lima and Cleni Mara Marzocchi-Machado and Luiz Fernando Fortunato Tucci and Antônio Carlos Alves De Sousa and Domingos de Jesus Rodrigues and Lucas Castro Fernandes Pimenta and Marcos Penhacek and Marcilei Juvenal da Conceição Horn and Jessyca Hathenher Gomes and Valéria Dornelles Gindri Sinhorin and Adilson Paulo Sinhorin},
journal = {Biology},
year = {2026},
month = oct,
doi = {10.3390/biology15191770},
url = {https://europepmc.org/article/MED/42883443},
note = {CC BY},
}
RIS
TY - JOUR
TI - Evaluation of Rhinella marina Extracts on the Effector Functions of Human Neutrophils.
AU - Lucinéia Reuse Albiero
AU - Valfran da Silva Lima
AU - Cleni Mara Marzocchi-Machado
AU - Luiz Fernando Fortunato Tucci
AU - Antônio Carlos Alves De Sousa
AU - Domingos de Jesus Rodrigues
AU - Lucas Castro Fernandes Pimenta
AU - Marcos Penhacek
AU - Marcilei Juvenal da Conceição Horn
AU - Jessyca Hathenher Gomes
AU - Valéria Dornelles Gindri Sinhorin
AU - Adilson Paulo Sinhorin
PY - 2026
DA - 2026/10/04
JO - Biology
DO - 10.3390/biology15191770
UR - https://europepmc.org/article/MED/42883443
AB - Neutrophils play a central role in the innate immune response. However, in inflammatory and autoimmune diseases, the exacerbated activation of these cells can result in excessive release of reactive oxygen species (ROS), proteases, and inflammatory mediators, contributing to tissue damage. In this context, natural compounds derived from amphibian venoms have attracted interest due to their pharmacological and immunomodulatory potential. This study aimed to evaluate in vitro the effects of the crude methanolic extract (CME) of Rhinella marina on the effector functions of human neutrophils. For this purpose, peripheral blood neutrophils from healthy individuals were treated with CME (0.5, 5, and 50 µg/mL) or untreated controls. Cytotoxicity, total ROS production, superoxide anion production, myeloperoxidase (MPO) activity, elastase degranulation, NET (Neutrophil Extracellular Trap) formation, and parameters related to cellular redox status, including antioxidant enzymes and markers of oxidative damage, were evaluated. CME showed concentration-dependent cytotoxicity. There were no changes in ROS production by luminol-dependent chemiluminescence after stimulation with myristoylphorbol acetate (PMA). However, it reduced superoxide anion production in neutrophils in both stimuli in the NBT assay. CME did not significantly modulate MPO activity or NET formation, but it reduced elastase release, suggesting modulation of neutrophil degranulation. Additionally, it increased glutathione-S-transferase (GST) activity and reduced glutathione (GSH) levels. It can be concluded that CME partially modulated neutrophil effector functions, such as superoxide anion production and degranulation, in addition to exhibiting partial protective effects on cellular redox state parameters. These findings suggest the extract's immunomodulatory potential and reinforce the need for further studies to clarify its mechanisms of action and possible applicability in neutrophil-mediated inflammatory conditions.
SN - 2079-7737
ER -