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Franciane Bobinski

Experimental Neuroscience Laboratory (LaNEx), Postgraduate Program in Health Sciences, University of Southern Santa Catarina (UNISUL), Palhoça, Brazil.

2 papers in the library · 18 citations · publishing 2025

Papers

Ayahuasca Pretreatment Prevents Sepsis-Induced Anxiety-Like Behavior, Neuroinflammation, and Oxidative Stress, and Increases Brain-Derived Neurotrophic Factor.

Molecular neurobiology May 1, 2025 Rick Wilhiam de Camargo, Larissa Joaquim, Richard Simon Machado et al. 13 citations

Pretreatment with the psychoactive decoction Ayahuasca (AYA) for three days before inducing sepsis in rats reduced anxiety-like behaviors and neuroinflammation. AYA increased time spent in the open arms of an elevated plus maze and prevented excessive grooming and rearing, indicating anxiolytic effects. It raised levels of the anti-inflammatory cytokine interleukin-4 in the prefrontal cortex and cortex and brain-derived neurotrophic factor in the cortex. AYA also increased myeloperoxidase activity in the prefrontal cortex and hippocampus while decreasing nitrite/nitrate concentrations across multiple brain regions, suggesting enhanced neutrophil activation and reduced nitric oxide signaling. Additionally, AYA prevented lipid peroxidation in the prefrontal cortex, hippocampus, and cortex. These findings suggest AYA may protect against sepsis-induced neuroinflammation, oxidative stress, and anxiety-like symptoms.

Ayahuasca reverses ischemic stroke-induced neuroinflammation and oxidative stress.

Behavioural brain research May 8, 2025 Larissa da Silva Joaquim, Lara Rodrigues da Rosa, Yasmin Strickert et al. 5 citations

Ayahuasca, a decoction containing β-carbolines and DMT, reversed stroke-induced increases in the inflammatory markers IL-6, IL-10, and MPO activity in the prefrontal cortex and hippocampus of rats, and reduced oxidative stress markers TBARS in the prefrontal cortex and hippocampus. It also modulated mitochondrial enzyme activity in the hippocampus and cortex. However, ayahuasca did not improve neurological deficits, locomotion, anxiety-like behavior, or recognition memory. These molecular changes suggest a neuroprotective role against ischemia-induced neuroinflammation and oxidative stress, though without corresponding functional improvements in this three-day treatment study.