ArticleNeurochemical research2025
Study on the Mechanism of Dihydromyricetin in Alleviating Depressive-Like Behavior in Rats Based on Network Pharmacology.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Exploration of Potential Antidepressant Active Ingredients ofJournal of analytical methods in chemistry · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Depression is a chronic and recurrent neuropsychiatric disorder with complex pathophysiology. Dihydromyricetin (DMY), a bioactive flavonoid compound isolated from Ampelopsis grossedentata (commonly known as rattan tea), has demonstrated multiple pharmacological properties including anti-inflammatory, antioxidant, antitumor, and antimicrobial activities. In the present study, a well-established rodent model of depression was generated through chronic unpredictable mild stress (CUMS) paradigm combined with social isolation. Following eight weeks of DMY intervention, comprehensive behavioral assessments were conducted to validate both the successful establishment of the depression model and the therapeutic efficacy of DMY treatment. We employed network pharmacology approaches to systematically predict potential antidepressant targets of DMY. Further mechanistic investigations were performed to elucidate the underlying molecular pathways, providing novel perspectives for developing innovative antidepressant therapeutics.Integrating network pharmacology prediction with molecular biology validation, our findings revealed that DMY exerts significant antidepressant-like effects through suppression of the advanced glycosylation end products (AGEs)-RAGE signaling pathway, activation of the nuclear factor E2-related factor 2 (NRF2)-mediated antioxidant defense system, and upregulation of synaptic plasticity-related proteins including postsynaptic density protein 95 (PSD95) and synaptophysin (SYP). These results suggest that DMY may represent a promising natural therapeutic candidate for depression treatment.
Indexed as
Identifiers
40418429What Socratic holds
Registered trials
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 Socratic graph.