ArticleNeuromolecular medicine2014
Attenuation of reserpine-induced pain/depression dyad by gentiopicroside through downregulation of GluN2B receptors in the amygdala of mice.
Article in Neuromolecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 69 citations in OpenAlex.
- Antidepressant-Like Effects ofPharmaceuticals (Basel, Switzerland) · 2026Article
- Scopoletin Attenuates Reserpine-Induced Pain-Depression Dyad in Mice via Modulation of Inflammation, Oxidative Stress, and Monoaminergic Pathways.Neuromolecular medicine · 2025Article
- Ginkgolide B as a biopsychosocial treatment salvages repeated restraint stress-induced amygdalar anomalies in mice.IBRO neuroscience reports · 2025Article
- Riboceine Regimen Circumvents Reserpine-Induced Hepatotoxicity via the Modulation of Key Liver Function Markers in Adult Male Wistar Rats.Archives of Razi Institute · 2025Article
- Article
- Therapeutic efficacy and mechanisms of gentiopicroside in various diseases.Frontiers in pharmacology · 2025Review
- Modulation of Brain-derived Neurotrophic Factor Expression by Physical Exercise in Reserpine-induced Pain-depression Dyad in Mice.Experimental neurobiology · 2024Article
- Glycitein prevents reserpine-induced depression and associated comorbidities in mice: modulation of lipid peroxidation and TNF-α levels.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Pathogenesis of depression and the potential for traditional Chinese medicine treatment.Frontiers in pharmacology · 2024Review
- Gentiopicroside-An Insight into Its Pharmacological Significance and Future Perspectives.Cells · 2023Review
- Therapeutic potential of plant iridoids in depression: a review.Pharmaceutical biology · 2022Review
- Preclinical reserpine models recapitulating motor and non-motor features of Parkinson's disease: Roles of epigenetic upregulation of alpha-synuclein and autophagy impairment.Frontiers in pharmacology · 2022Article
- Skimmetin/osthole mitigates pain-depression dyad via inhibiting inflammatory and oxidative stress-mediated neurotransmitter dysregulation.Metabolic brain disease · 2021Article
- Relevance of Mitochondrial Dysfunction in the Reserpine-Induced Experimental Fibromyalgia Model.Molecular neurobiology · 2020Article
- Traditional Chinese Medicine in Depression Treatment: From Molecules to Systems.Frontiers in pharmacology · 2020Review
- Potential of animal models for advancing the understanding and treatment of pain in Parkinson's disease.NPJ Parkinson's disease · 2020Review
- Gentiopicroside abrogates lipopolysaccharide-induced depressive-like behavior in mice through tryptophan-degrading pathway.Metabolic brain disease · 2018Article
- Effect of ZBD-2 on chronic pain, depressive-like behaviors, and recovery of motor function following spinal cord injury in mice.Behavioural brain research · 2017Article
- Spontaneously Hypertensive Rats (SHR) Are Resistant to a Reserpine-Induced Progressive Model of Parkinson's Disease: Differences in Motor Behavior, Tyrosine Hydroxylase and α-Synuclein Expression.Frontiers in aging neuroscience · 2017Article
- Echinocystic acid reduces reserpine-induced pain/depression dyad in mice.Metabolic brain disease · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological studies demonstrate that pain frequently occurs comorbid with depression. Gentiopicroside (Gent) is a secoiridoid compound isolated from Gentiana lutea that exhibits analgesic properties and inhibits the expression of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors in the anterior cingulate cortex of mice. However, the effects of Gent on the reserpine-induced pain/depression dyad and its underlying mechanisms are unclear. Reserpine administration (1 mg/kg subcutaneous daily for 3 days) caused a significant decrease in the nociceptive threshold as evidenced by the reduced paw withdrawal latency in response to a radiant heat source and mechanical allodynia. Behavioral detection indicated a significant increase in immobility time during a forced swim test, as well as decreased time in the central area and total travel distance in an open field test. Furthermore, reserpinized animals exhibited increased oxidative stress. Systemic Gent administration dose-dependently ameliorated the behavioral deficits associated with reserpine-induced pain/depression dyad. At the same time, the decrease in biogenic amine levels (norepinephrine, dopamine, and serotonin) was integrated with the increase in caspase-3 levels and GluN2B-containing NMDA receptors in the amygdala of the reserpine-injected mice. Gent significantly reversed the changes in the levels of biogenic amines, caspase-3, and GluN2B-containing NMDA receptors in amygdala. However, Gent did not affect the expression of GluN2A-containing NMDA receptors. The inhibitory effects of Gent on oxidative stress were occluded by simultaneous treatment of GluN2B receptors antagonist Ro25-6981. Our study provides strong evidence that Gent inhibits reserpine-induced pain/depression dyad by downregulating GluN2B receptors in the amygdala.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.