ArticleInternational journal of molecular sciences2024
Network Pharmacology and Transcriptomics to Explore the Pharmacological Mechanisms of 20(S)-Protopanaxatriol in the Treatment of Depression.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Article
- Integrated WGCNA and Network Pharmacology Explore the Potential Mechanisms of D-Limonene in Alleviating Traumatic Brain Injury.International journal of molecular sciences · 2026Article
- Association between miR-182 rs76481776 Polymorphism and Antidepressant Treatment Response in Patients with Depression.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026Article
- Optimization of potential targets for antidepressant Chinese medicines: AI and multi-omics methods.Chinese medicine · 2026Review
- Associations Between Social Jetlag and Gut Microbiome Profiles in Adolescents.Nature and science of sleep · 2026Article
- Quercetin and Citreorosein fromCurrent pharmaceutical design · 2026Article
- Pharmacokinetics and pharmacological activities of protopanaxatriol.Journal of ginseng research · 2025Review
- Network Pharmacology-Driven Sustainability: AI and Multi-Omics Synergy for Drug Discovery in Traditional Chinese Medicine.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Neuroprotective Terpenoids Derived fromInternational journal of molecular sciences · 2025Article
- Huaxian formula alleviates nickel oxide nanoparticle-induced pulmonary fibrosis via PI3K/AKT signaling.Scientific reports · 2025Article
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10 authors.
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Abstract
Depression is one of the most common psychological disorders nowadays. Studies have shown that 20(S)-protopanaxatriol (PPT) can effectively improve depressive symptoms in mice. However, its mechanism needs to be further explored. In this study, we used an integrated approach combining network pharmacology and transcriptomics to explore the potential mechanisms of PPT for depression. First, the potential targets and pathways of PPT treatment of depression were screened through network pharmacology. Secondly, the BMKCloud platform was used to obtain brain tissue transcription data of chronic unpredictable mild stress (CUMS) model mice and screen PPT-altered differential expression genes (DEGs). Gene ontology (GO) analysis and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed using network pharmacology and transcriptomics. Finally, the above results were verified by molecular docking, Western blotting, and quantitative real-time polymerase chain reaction (qRT-PCR). In this study, we demonstrated that PPT improved depression-like behavior and brain histopathological changes in CUMS mice, downregulated nitric oxide (NO) and interleukin-6 (IL-6) levels, and elevated serum levels of 5-hydroxytryptamine (5-HT) and brain-derived neurotrophic factor (BDNF) after PPT treatment compared to the CUMS group. Eighty-seven potential targets and 350 DEGs were identified by network pharmacology and transcriptomics. Comprehensive analysis showed that transthyretin (TTR), klotho (KL), FOS, and the phosphatidylinositol 3-kinase-protein kinase B (PI3K-AKT) signaling pathway were closely associated with the therapeutic effects of PPT. Molecular docking results showed that PPT had a high affinity for PI3K, AKT, TTR, KL, and FOS targets. Gene and protein level results showed that PPT could increase the expression of PI3K, phosphorylation of PI3K (p-PI3K), AKT, phosphorylation of AKT (p-AKT), TTR, and KL and inhibit the expression level of FOS in the brain tissue of depressed mice. Our data suggest that PPT may achieve the treatment of depression by inhibiting the expression of FOS, enhancing the expression of TTR and KL, and modulating the PI3K-AKT signaling pathway.
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