ArticleJournal of neural transmission (Vienna, Austria : 1996)2008
The anthraquinone derivative Emodin ameliorates neurobehavioral deficits of a rodent model for schizophrenia.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 35 citations in OpenAlex.
- Schizophrenia Animal Modeling with Epidermal Growth Factor and Its Homologs: Their Connections to the Inflammatory Pathway and the Dopamine System.Biomolecules · 2023Review
- Therapeutic benefits of prophetic medicine remedies in treating hematological diseases (A review article).American journal of blood research · 2023Review
- Alternative Therapy of Psychosis: Potential Phytochemicals and Drug Targets in the Management of Schizophrenia.Frontiers in pharmacology · 2022Review
- Emodin Protects SH-SY5Y Cells Against Zinc-Induced Synaptic Impairment and Oxidative Stress Through the ERK1/2 Pathway.Frontiers in pharmacology · 2022Article
- Resting-state dopaminergic cell firing in the ventral tegmental area negatively regulates affiliative social interactions in a developmental animal model of schizophrenia.Translational psychiatry · 2021Article
- Neuroprotective effect of emodin against Alzheimer's disease via Nrf2 signaling in U251 cells and APP/PS1 mice.Molecular medicine reports · 2021Article
- Establishing GPCR Targets of hMAO Active Anthraquinones fromACS omega · 2020Article
- Clozapine-dependent inhibition of EGF/neuregulin receptor (ErbB) kinases.Translational psychiatry · 2019Article
- Nutraceuticals against Neurodegeneration: A Mechanistic Insight.Current neuropharmacology · 2016Review
- ErbB inhibitors ameliorate behavioral impairments of an animal model for schizophrenia: implication of their dopamine-modulatory actions.Translational psychiatry · 2013Article
- ErbB1-4-dependent EGF/neuregulin signals and their cross talk in the central nervous system: pathological implications in schizophrenia and Parkinson's disease.Frontiers in cellular neuroscience · 2013Article
- Csnk1e is a genetic regulator of sensitivity to psychostimulants and opioids.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Article
- Neuroprotection by spice-derived nutraceuticals: you are what you eat!Molecular neurobiology · 2011Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormality in cytokine signaling is implicated in the neuropathology of schizophrenia. Previously, we established an animal model for schizophrenia by administering epidermal growth factor (EGF) to neonatal rats. Here we investigated effects of the anthraquinone derivatives emodin (3-methyl-1,6,8-trihydroxyanthraquinone) and sennoside (bis-[D: -glucopyranosyl-oxy]-tetrahydro-4,4'-dihydroxy-dioxo[bianthracene]-2,2'-dicarboxylic acid) on behaviors of this model and EGF signaling. Subchronic oral administration of emodin (50 mg/kg) suppressed acoustic startle responses and abolished prepulse inhibition (PPI) deficits in this rodent model. ANCOVA revealed that emodin had distinct effects on PPI and startle responses. In contrast, sennoside (50 mg/kg) had no effects. Emodin attenuated weight gain initially during treatment but had no apparent effect on weight gain and locomotor activity thereafter. Application of emodin to neocortical cultures attenuated the phosphorylation of ErbB1 and ErbB2. We conclude that emodin can both attenuate EGF receptor signaling and ameliorate behavioral deficits. Therefore, emodin might be a novel class of a pro-drug for anti-psychotic medication.
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