Objectives: Kaixinsan (KXS), a traditional Chinese medicine formula, has been demonstrated to be effective in the treatment of depression. The present study applied a network pharmacology approach to dig out the new targets and mechanism of action of KXS and the active compounds in the treatment of depression.
Methods: A network pharmacology approach based on public databases including ADME (absorption, distribution, metabolism, and excretion) evaluation, targets prediction, construction of networks, and molecule docking was used and validated the predicted new antioxidant targets and mechanisms in vitro. Based on an in vitro experiment, we verified the AKT1/Nrf2 pathway related to the thioredoxin (Trx) antioxidant mechanism.
Results: The present study sorted 31 pharmacologically active components (kaempferol, ginsenoside rh2, ginsenoside rh4, stigmasterol, etc.) through the ADME algorithm from KXS. 136 potential molecular targets (AKT1, TNF, IL-1b, JUN, ESR1, NOS3, etc.) were predicted, of which there were 69 targets clearly related to depression. By compound-depression targets (C-DTs) network constructed, and protein-protein interaction networks (PPI) and KEGG pathway enrichment analyzed, we identified active compounds mediating depression-related targets to exert synergism on the predictive AKT1/Nrf2 pathway related to thioredoxin (Trx) antioxidant mechanism and other inflammation-related signaling pathways as well as neurotransmitter related signaling pathways. In the HO induced SH-SY5Y cell damage model, this showed kaempferol and ginsenoside rh2 could enhance the activity of the Trx system by upregulation of AKT1 to activate Nrf2 in vitro.
Conclusions: Taken together, by comprehensive systems pharmacology approach analysis, we found that KXS and its active compounds might exhibit antioxidant effects by stimulating the AKT1/Nrf2 pathway in the treatment of depression, which might shed new light on innovative therapeutic tactics for the new aspects for depression in traditional Chinese medicine in future studies.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9325646 | PMC |
| http://dx.doi.org/10.1155/2022/7302442 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Comparative antibacterial activity of clove extract against Pseudomonas aeruginosa.
BMC Complement Med Ther
January 2025
Department of Faculty of Health Sciences, American University of Madaba, Madaba, Jordan.
Pseudomonas aeruginosa is an opportunistic pathogen belonging to the γ-proteobacteria family, known to cause pneumonia linked with ventilator use and nosocomial infections. With the increasing prevalence of antibiotic-resistant bacteria, there is a pressing need to identify alternatives to conventional antibiotics. Plant-derived substances (PDSs) offer potential not only as antibacterial agents but also as modulators of antibiotic resistance.
View Article and Find Full Text PDFFailure to repair damaged NAD(P)H blocks de novo serine synthesis in human cells.
Cell Mol Biol Lett
January 2025
Enzymology and Metabolism Group, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, L-4367, Belvaux, Luxembourg.
Background: Metabolism is error prone. For instance, the reduced forms of the central metabolic cofactors nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotide phosphate (NADPH), can be converted into redox-inactive products, NADHX and NADPHX, through enzymatically catalyzed or spontaneous hydration. The metabolite repair enzymes NAXD and NAXE convert these damaged compounds back to the functional NAD(P)H cofactors.
View Article and Find Full Text PDFBioprocess development for microbial production and purification of cellobiose lipids by the smut fungus Ustilago maydis DSM 4500.
Bioprocess Biosyst Eng
January 2025
Department of Chemical Engineering, Stellenbosch University, Private Bag X1, Matieland, 7602, South Africa.
Cellobiose lipids (CBLs) are a class of glycolipid biosurfactants produced by various fungal strains. These compounds have gained significant interest due to their surface-active and antifungal properties, which are comparable to traditional synthetic surfactants and antimicrobials. Despite their potential applicability in various cosmetic, pharmaceutical, and agricultural formulations, significantly less research has been focused on their production and purification in comparison to other glycolipid biosurfactants, such as mannosylerythritol lipids (MELs) and sophorolipids.
View Article and Find Full Text PDFBone marrow transplantation reverses metabolic alterations in multiple sulfatase deficiency: a case series.
Commun Med (Lond)
January 2025
Department of Pediatrics, Division of Blood and Marrow Transplantation, University of Minnesota, Minneapolis, MN, USA.
Background: Multiple sulfatase deficiency (MSD) is an exceptionally rare neurodegenerative disorder due to the absence or deficiency of 17 known cellular sulfatases. The activation of all these cellular sulfatases is dependent on the presence of the formylglycine-generating enzyme, which is encoded by the SUMF1 gene. Disease-causing homozygous or compound heterozygous variants in SUMF1 result in MSD.
View Article and Find Full Text PDFInfluence of ABCB1 polymorphisms on aripiprazole and dehydroaripiprazole plasma concentrations.
Sci Rep
January 2025
Pharmacy Department, University Clinical Hospital of Santiago de Compostela (SERGAS), 15706, Santiago de Compostela, Spain.
Aripiprazole (ARI) is an atypical antipsychotic which is a substrate of P-glycoprotein (P-gp), a transmembrane glycoprotein that plays a crucial role in eliminating potentially harmful compounds from the organism. ARI once-monthly (AOM) is a long-acting injectable form which improves treatment compliance. Genetic polymorphisms in ABCB1 may lead to changes in P-gp function, leading to individual differences in drug disposition.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!