ArticleFrontiers in neuroscience2020
Postnatal Antioxidant and Anti-inflammatory Treatments Prevent Early Ketamine-Induced Cortical Dysfunctions in Adult Mice.
Article in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Targeting beta-2 adrenergic receptor attenuates schizophrenia-like behavioral effects induced by ketamine in mice: cAMP/PKA/BDNF-PEA-3 and RIM-1α signaling pathways involvement.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026Article
- Eugenol mitigates schizophrenia-like behavioral deficits, oxidative stress, apoptosis, neuroinflammation, and cholinergic dysfunction in ketamine-induced mice.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- Exploratory Analysis of MicroRNA Alterations in a Neurodevelopmental Mouse Model for Autism Spectrum Disorder and Schizophrenia.International journal of molecular sciences · 2024Article
- The Therapeutic Potential of Celastrol in Central Nervous System Disorders: Highlights from In Vitro and In Vivo Approaches.Molecules (Basel, Switzerland) · 2021Review
- N-3 PUFA Prevent Oxidative Stress in a Rat Model of Beta-Amyloid-Induced Toxicity.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Enhancement of Oxytocin in the Medial Prefrontal Cortex Reverses Behavioral Deficits Induced by Repeated Ketamine Administration in Mice.Frontiers in neuroscience · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early brain insult, interfering with its maturation, may result in psychotic-like disturbances in adult life. Redox dysfunctions and neuroinflammation contribute to long-term psychiatric consequences due to neurodevelopmental abnormalities. Here, we investigated the effects of early pharmacological modulation of the redox and inflammatory states, through celastrol, and indomethacin administration, on reactive oxygen species (ROS) amount, levels of malondialdehyde (MDA) and antioxidant enzymes (superoxide dismutase 1, SOD1, glutathione, GSH, and catalase, CAT), as well as of pro-inflammatory cytokines (tumor necrosis factor-alpha, TNF-α, interleukin-6, IL-6, and interleukin-1 beta, IL-1β), in the prefrontal cortex of adult mice exposed to a neurotoxic insult, i.e. ketamine administration, in postnatal life. Early celastrol or indomethacin prevented ketamine-induced elevations in cortical ROS production. MDA levels in ketamine-treated mice, also administered with celastrol, were comparable with the control ones. Indomethacin also prevented the increase in lipid peroxidation following early ketamine administration. Whereas no significant differences were detected in SOD1, GSH, and CAT levels between ketamine and saline-administered mice, celastrol elevated the cortical amount of these antioxidant enzymes and the same effect was induced by indomethacin
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