Current protein & peptide science · 2026
Phα1β, a Peptide Derived from the Spider Phoneutria nigriventer, is a Potential New Antioxidant and Inflammation Modulator.
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Nogueira-Machado José Augusto, Rocha-Silva Fabiana, Jordão Debora Siqueira, Cassanje Adriano Dala, Gomez Marcus Vinicius
Аннотация
BACKGROUND: The peptide Phα1β, derived from the venom of Phoneutria nigriventer, has been extensively investigated for its antinociceptive properties, primarily associated with modulation of ion channels and inflammatory pathways. However, its effects on oxidative stress and immune cell function remain incompletely understood.
OBJECTIVE: This study aimed to investigate the effects of recombinant Phα1β (rPhα1β) on Reactive Oxygen Species (ROS) production and inflammatory mediator release in human immune cells.
METHODS: Human neutrophils were isolated and stimulated to evaluate ROS production using a luminol-dependent chemiluminescence assay. The involvement of the protein kinase C (PKC) pathway was assessed using pharmacological modulators, including phorbol dibutyrate (PDB) and calphostin C. Cytokine levels were measured to determine the impact of rPhα1β on inflammatory responses.
RESULTS: rPhα1β significantly reduced ROS production in human neutrophils. This effect was comparable to that observed with PKC inhibition and was reversed by PKC activation, suggesting modulation of the PKC/NADPH oxidase axis. In parallel, rPhα1β markedly decreased IL-6 levels, while exerting minimal effects on IL-4 and IL-10. Additionally, modulation of CCR5-related signaling was observed, indicating a potential effect on chemokine-mediated inflammatory pathways.
CONCLUSION: These findings demonstrate that rPhα1β acts as a modulator of oxidative stress and inflammatory signaling in human immune cells. Its ability to reduce ROS production and selectively inhibit pro-inflammatory mediators suggests a mechanism involving the PKC/NADPH oxidase pathway. This study expands the current understanding of venom-derived peptides and highlights rPhα1β as a promising candidate for targeting redox-dependent inflammatory processes.
OBJECTIVE: This study aimed to investigate the effects of recombinant Phα1β (rPhα1β) on Reactive Oxygen Species (ROS) production and inflammatory mediator release in human immune cells.
METHODS: Human neutrophils were isolated and stimulated to evaluate ROS production using a luminol-dependent chemiluminescence assay. The involvement of the protein kinase C (PKC) pathway was assessed using pharmacological modulators, including phorbol dibutyrate (PDB) and calphostin C. Cytokine levels were measured to determine the impact of rPhα1β on inflammatory responses.
RESULTS: rPhα1β significantly reduced ROS production in human neutrophils. This effect was comparable to that observed with PKC inhibition and was reversed by PKC activation, suggesting modulation of the PKC/NADPH oxidase axis. In parallel, rPhα1β markedly decreased IL-6 levels, while exerting minimal effects on IL-4 and IL-10. Additionally, modulation of CCR5-related signaling was observed, indicating a potential effect on chemokine-mediated inflammatory pathways.
CONCLUSION: These findings demonstrate that rPhα1β acts as a modulator of oxidative stress and inflammatory signaling in human immune cells. Its ability to reduce ROS production and selectively inhibit pro-inflammatory mediators suggests a mechanism involving the PKC/NADPH oxidase pathway. This study expands the current understanding of venom-derived peptides and highlights rPhα1β as a promising candidate for targeting redox-dependent inflammatory processes.