ArticleCombinatorial chemistry & high throughput screening2023
Network Pharmacology Study on the Mechanism of Gastrodin Reversing Depressive Symptoms in Traumatically Stressed Rats.
Article in Combinatorial chemistry & high throughput screening, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Metabolomics and Network Pharmacology Analyses Reveal the Mechanism of Moxibustion in Knee Osteoarthritis.Combinatorial chemistry & high throughput screening · 2026Article
- Food and medicine homology: a potential nutritional intervention strategy for post-acute COVID-19 syndrome.Frontiers in pharmacology · 2025Review
- Gastrodin, a Promising Natural Small Molecule for the Treatment of Central Nervous System Disorders, and Its Recent Progress in Synthesis, Pharmacology and Pharmacokinetics.International journal of molecular sciences · 2024Review
- Gastrodin improves nerve cell injury and behaviors of depressed mice through Caspase-3-mediated apoptosis.CNS neuroscience & therapeutics · 2024Article
- Integrating Network Pharmacology, Molecular Docking and Pharmacological Evaluation for Exploring theDrug design, development and therapy · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDepression is a typical outcome of the repair of posttraumatic stress disorder (PTSD). Based on network pharmacology and neuropharmacology experiments, this study aimed to explore how gastrodin (GAS) reverses depressive symptoms in traumatically stressed rats.
methodsGAS-related targets were predicted by SwissTargetPrediction; depression-related targets were collected from GeneCards and therapeutic target database (TTD); protein-protein interaction (PPI) network was constructed with its action mechanism being predicted by gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. The animal model of PTSD was replicated by single prolonged stress (SPS). The antidepressant effect of GAS was investigated by the forced swim test (FST) and tail suspension test (TST). The levels of tyrosine hydroxylase (TH) and corticotropin-releasing factor type I receptor (CRF1) in locus ceruleus (LC) and the expression of corticotropin-releasing factor (CRF) in the paraventricular nucleus of the hypothalamus (PVN) and central amygdala (CeA) were measured by immunofluorescence.
resultsGAS significantly shortened the tail suspension and swimming immobility in SPS rats in TST and FST experiments (p < 0.05 or p < 0.01). The network analysis showed that the critical antidepressant targets of GAS were 86 targets such as GAPDH, CASP3 MMP9, HRAS, DPP4, and TH, which were significantly enriched in the pathways such as pathways neuroactive ligandreceptor interaction. High doses of GAS could significantly reduce the level of TH and CRF in CEA in the brain of rats with depressive symptoms (p < 0.01) and, at the same time, lower the expression of CRF in PVN (p < 0.05).
conclusionThe effect of GAS on depressive symptoms in SPS rats may be closely related to its reduction of CRF expression in PVN and CeA and inhibition of neuron (NE) synthesis in LC.
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