ArticleBioMedicine2025
Neuroprotection of paeoniflorin as antidepressant candidate.
Article in BioMedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Depression is one of the common mental disorders worldwide, and currently used antidepressants have undesirable effects; therefore, the development of new antidepressants without side effects is urgently needed. Paeoniflorin (PF) exhibits various pharmacological activities, including anti-inflammatory, antioxidant, and neuroprotective effects. NMDA receptors in the hippocampus play a vital role in the pathophysiology of depression. Due to the scarcity of reports on the neuroprotection of PF on NMDA-induced excitotoxicity in the hippocampus, the present study aims to investigate the effects of PF on NMDA-mediated EPSP and calcium influx in the hippocampus to evaluate the potential of PF as an antidepressant. Methods: In order to investigate the effects of PF on the NMDA receptor in the hippocampus, the hippocampal slices, primary-cultured hippocampal neurons, and Results: PF (2 μM) significantly depressed the NMDA-mediated EPSPs, resulting in a 50 % inhibition. The intracellular calcium level in primary-cultured hippocampal neurons was 102.67 nM, and 520.36 nM after NMDA (125 μM) treatment. With NMDA and PF co-treatment, the calcium level was 204.58 μM, showing a 60.68 % decrease. After NMDA was co-treated with 1 μM ruthenium red (RuR), the calcium level increased (from 534.58 nM to 665.68 nM). Additionally, co-treatment with PF significantly decreased the calcium level (468.05 nM, representing a 29.50 % decrease). In the presence of NMDA and 1 μM ω-conotoxin MVIIC (ω-Cono) co-treatment, the calcium level was 496.29 nM. In the presence of NMDA, ω-Cono, and RuR, the calcium level was 568.5 nM. Additionally, NMDA, ω-Cono, RuR, and PF co-treatment significantly decreased the calcium level to 270.94 nM. In silico molecular docking analysis revealed a binding energy of -48.5188 kcal/mol for PF with the NMDA receptor. Conclusions: PF binds to the NMDA receptor, exhibits neuroprotection, and contributes to its potential as an antidepressant.
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