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Ayahuasca reverses ischemic stroke-induced neuroinflammation and oxidative stress.

Larissa da Silva Joaquim, Lara Rodrigues da Rosa, Yasmin Strickert, Richard Simon Machado, Everton Lanzzarin, Gabriela Bernardes, Suelen de Souza Ramos, Linério Ribeiro de Novais, Beatriz Steiner, Brenno Farias, Khiany Mathias, Helena Mafra Martins, Elisa Mitkus Flores Lins, Jéssica Schaefer Chaves, Douglas Camilo, Larissa Espindola da Silva, Mariana Pacheco de Oliveira, Mariella Reinol da Silva, Pablo Michel Pereira Barcelos, Fabiana Pereira Santos, Franciane Bobinski, Gislaine Tezza Rezin, Mauricio Yonamine, Antonio Inserra, Fabricia Petronilho, Rafael Mariano de Bitencourt

Behavioural Brain Research May 8, 2025 DOI: 10.1016/j.bbr.2025.115521 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Animal experiment Peer reviewed
Population Wistar rats subjected to middle cerebral artery occlusion model of ischemic stroke
Intervention Ayahuasca
Dose 2 and 4 mL/kg
Duration 3-day treatment, 72-hour post-stroke assessment
Topics Ayahuasca DMT
Keywords Ischemic stroke Neuroinflammation Neuroprotection Oxidative stress #ayahuasca traditional medicine Psychedelic brew #neuroprotectiveagents brain protection Neural defense #ischemicstroke brain ischemia
Citations 5
Key findings Ayahuasca treatment after ischemic stroke reduced neuroinflammation and oxidative stress in specific brain regions but did not improve neurological or behavioral outcomes.

Abstract

Ischemic stroke is a leading cause of death and disability worldwide. Survivors face disability and psychiatric sequelae resulting from ischemia-induced cell death and associated neuroinflammation, and oxidative stress. Herbal medicines have been shown to elicit neuroprotective effects following stroke due to their anti-inflammatory and antioxidant effects. Preliminary evidence suggests that Ayahuasca (AYA), a decoction made from the vine Banisteriopsis caapi containing β-carbolines and the shrub Psychotria viridis containing N, N-Dimethyltryptamine, might attenuate ischemia-induced neuroinflammation and oxidative stress. Therefore, in this study we investigated the putative protective effects of AYA in the middle cerebral artery occlusion (MCAO) model of ischemic stroke. Wistar rats were subjected to the MCAO stroke model or sham surgery on day 0. After 24-h, rats were treated for three days with AYA (2 and 4 mL/kg, gavage) or saline. Neurological score was assessed for 72-h post-stroke. Rats were tested in the elevated plus maze, open field, and novel object recognition tests to assess locomotion, anxiety-like behavior, and recognition memory. Interleukin (IL)-6, IL-10 myeloperoxidase (MPO) activity, and the nitrite/nitrate (N/N) concentrations were determined in the prefrontal cortex (PFC), hippocampus (HPC), hypothalamus (HYP) and cortex. as markers of inflammation. Oxidative stress was quantified in the same brain areas as measured by the levels of thiobarbituric acid reactive species (TBARS), protein carbonylation, and superoxide dismutase (SOD), and catalase (CAT) activity. Mitochondrial metabolism was assessed quantifying the activity of complex 1(CI), CII, citrate synthase (CS), succinate dehydrogenase (SDH), and creatine kinase (CK). No differences were observed regarding neurological deficits, locomotion, anxiety-like behavior, and recognition memory. However, AYA reversed the stroke-induced increase in IL-6 levels in the PFC and the HPC, IL-10 in the PFC, HPC, and HYP, MPO activity in the PFC, and N/N concentration and CAT activity in the HYP. Moreover, AYA decreased TBARS levels in the PFC and HPC and brain-derived neurotrophic factor (BDNF) in the PFC, and increased SOD activity in the cortex. Lastly, AYA increased CI activity in the HPC and cortex and decreased SDH and CK activity in the HPC. AYA administration following ischemic stroke modulates oxidative stress and neuroinflammation in the PFC, HPC, and HYP. Despite no significant improvements in neurological or behavioral scores, these molecular changes suggest a neuroprotective role of AYA. Future studies should explore the timing of AYA treatment and putative long-term effects on functional recovery, as well as its potential in other brain regions critical for cognitive and motor functions.

Comparable studies

Other preclinical and animal studies on ayahuasca, most cited first.

Study Year Design Participants
Monoamine oxidase inhibitors in South American hallucinogenic plants: Tryptamine and β-carboline constituents of Ayahuasca Eight ayahuasca samples from Peru and several Banisteriopsis caapi cultivars 1984 Qualitative and quantitative chemical analysis with in vitro assay
The alkaloids of Banisteriopsis caapi, the plant source of the Amazonian hallucinogen Ayahuasca, stimulate adult neurogenesis in vitro Progenitor cells from subventricular and subgranular zones of adult mice brains 2017 In vitro experimental study
N,N-dimethyltryptamine compound found in the hallucinogenic tea ayahuasca, regulates adult neurogenesis in vitro and in vivo Mice 2020 In vitro and in vivo experimental study
Behavioural and neurotoxic effects of ayahuasca infusion (Banisteriopsis caapi and Psychotria viridis) in female Wistar rat Female Wistar rats 2015 Observational cohort
Effects of ayahuasca on the development of ethanol-induced behavioral sensitization and on a post-sensitization treatment in mice Mice 2015 Experimental study

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