Mechanism of quercetin in the treatment of endometriosis based on network pharmacology and transcriptome sequencing
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1184737 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31308200_1.fastq.gz | Fastqsanger.gz | |||
| SRR31308200_2.fastq.gz | Fastqsanger.gz | |||
| SRR31308201_1.fastq.gz | Fastqsanger.gz | |||
| SRR31308201_2.fastq.gz | Fastqsanger.gz | |||
| SRR31308202_1.fastq.gz | Fastqsanger.gz |
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Project description:This study explores how quercetin may treat endometriosis (EMs) by combining network pharmacology and transcriptome sequencing approaches. Through network pharmacology, 132 shared targets between quercetin and EMs were identified, with KEGG pathway analysis suggesting that the MAPK signaling pathway could be a significant therapeutic target. Transcriptome sequencing revealed that PDGFRB was highly expressed in ectopic endometrial tissue, a finding confirmed by immunohistochemistry (IHC) showing elevated levels of PDGFRB, RAS, RAF1, and ERK1/2 in ectopic lesions. In an EMs mouse model, quercetin treatment led to a marked reduction in ectopic lesion volume, lowered adhesion scores, and decreased expression of PDGFRB, RAS, RAF1, and ERK1/2 in endometrial tissues. Additionally, the knockdown of PDGFRB in endometriosis cells inhibited their proliferation, invasion, and migration, processes critical to EMs pathology. Quercetin treatment further suppressed cell viability and downregulated the protein expression of RAS, phosphorylated RAF1, RAF1, phosphorylated ERK, and ERK1/2. These findings collectively suggest that quercetin exerts its therapeutic effect in endometriosis by regulating the MAPK signaling pathway via PDGFRB, thereby reducing EMs cell proliferation, invasion, and migration. This study provides insights into quercetin’s multi-targeted mechanism of action in endometriosis treatment.
2024-11-16 | GSE281569 | GEO
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Project description:Risperidone is an atypical antipsychotic that can cause substantial weight gain. The pharmacological targets and molecular mechanisms related to risperidone-induced lipogenesis (RIL) remain to be elucidated. Therefore, network pharmacology and further experimental validation were undertaken to explore the action mechanisms of RIL. In this study, RIL was systematically analyzed using integrating multiple databases through integrated network pharmacology, transcriptomics, molecular docking, and molecular experiment analysis. The potential signaling pathways for RIL were identified and experimentally validated using Gene Ontology (GO) enrichment and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Our experimental data showed that Risperidone promotes adipocyte differentiate and lipid accumulation. And network pharmacology and GO analyses showed that risperidone induced adipocyte metabolism, differentiation, and lipid accumulation related functions. Intersecting analysis, molecular docking, and pathway validation analysis indicated that risperidone activated adipocytokine signaling pathway related genes by targeting MAPK14 (Mitogen-activated protein kinase 14), MAPK8 (Mitogen-activated protein kinase 8), and RXRA (Retinoic acid receptor RXR-alpha), thereby inhibiting long-chain fatty acid beta-oxidation by suppressing STAT3 (Signal transducer and activator of transcription 3) expression and phosphorylation. This study suggested that Risperidone increases adipocyte lipid accumulation by plausible inhibiting long-chain fatty acid beta-oxidation through targeting MAPK14, MAPK8, and RXRA.
2022-05-11 | GSE198053 | GEO
Project description:<p>Background: Triple-negative breast cancer (TNBC) urgently needs effective therapies due to limited targeted options and unfavorable outcomes. We investigated Trichosanthes kirilowii Maxim formula granules (TKM) using integrated network pharmacology, metabolomics, and molecular pharmacology to clarify potential multi-target mechanisms relevant to TNBC.</p><p>Methods: Liquid chromatography coupled with mass spectrometry was employed to identify the components of TKM formula granules. Network pharmacology-based prediction was used to uncover potential mechanisms by which TKM counteracts TNBC. Potential targets were identified, and pathway enrichment analysis was performed. Subsequently, TNBC cells and 4T1 tumor-bearing mice were used to verify the molecular mechanisms of TKM.</p><p>Results: We identified 151 active compounds in TKM. Through network pharmacology analysis, 214 TNBC-related targets were found, with 28 core targets, including cell cycle and apoptosis regulators MYC, TP53, AKT1, CCND1, CASP3, PIK3CA, BCL2L1, and CDC42. The compound-target-pathway-disease network showed that schisandrin binds to many treatment targets with satisfactory docking performance, especially for MYC and AKT1. Experimentally, TKM was found to significantly promote apoptosis and induce G2/M-phase cell-cycle arrest in MDA-MB-231 cells. Western blot analysis showed that TKM suppressed PI3K/AKT and Wnt/β-catenin signaling pathways. Surface plasmon resonance experiment revealed that schisandrin binds to recombinant AKT1 with an equilibrium dissociation constant (K_D) of 0.1525 mM. According to untargeted metabolomics results, TKM can regulate amino acid, glycine, serine, and threonine metabolism, mineral absorption, protein digestion and absorption, central carbon metabolism, and arginine biosynthesis to exert therapeutic effects on TNBC. All findings were consistent with predicted targets and pathways.</p><p>Conclusion: This study comprehensively explores the multi-target mechanisms of TKM against TNBC using network pharmacology, molecular pharmacology, and metabolomics approaches. These findings provide a foundation for future mechanistic investigations and may support the further preclinical development of TKM-based strategies for TNBC.</p>
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Project description:Objective: This study combines transcriptomics and network pharmacology to explore the mechanism of action of Jia Wei Xing Bi Gel nasal drops in treating allergic rhinitis (AR) in children. Methods: A total of 56 AR children were randomly divided into Jia Wei Xing Bi Gel nasal drops(JWXBGND) group and mometasone furoate nasal spray (MFGS) group, with 28 cases in each group, and a healthy control group of 20 cases. After 4 weeks of treatment, efficacy was evaluated, and RNA-seq, database mining, and bioinformatics analysis methods were employed. Results: In terms of clinical efficacy, the TCM group showed better improvement in nasal itching, ocular symptoms, non-nasal ocular symptoms, and behavioral issues compared to the western medicine group, with a more significant decrease in TCM syndrome scores; transcriptomic analysis revealed 2776 differentially expressed genes when comparing AR children with healthy children, and 441 differential genes were identified between JWXBGND group and MFGS group; combined analysis of transcriptomics and network pharmacology identified 195 active components and 493 targets of action for Jiawei Xingbi Gel, with core components including ferulic acid, fexofenadine, and curcumin A, and core targets involving TNF, IL-6, IL-1β, AKT1, ALB, SRC, etc.; KEGG pathway analysis mainly enriched in caffeine metabolism, linoleic acid metabolism, Th17 cell differentiation, HIF-1 signaling pathway, etc.; molecular docking results indicated that key active components of Jia Wei Xing Bi Gel nasal drops bind stably to targets such as ALB, AKT1, SRC, TP53, etc. Conclusion: Jia Wei Xing Bi Gel nasal drops can effectively alleviate AR symptoms, and its mechanism may be related to the regulation of inflammatory signaling pathways through multiple components and multiple targets
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Project description:Jiawei Foshou San (JFS) is the new formula originated from classic Foshou San formula, composed with ligustrazine, ferulic acid, and tetrahydropalmatine. Previously JFS inhibited the growth of endometriosis (EMS) with unclear mechanism, especially in metastasis, invasion, and epithelial-mesenchymal transition. In this study, network pharmacology was performed to explore potential mechanism of JFS on EMS. Through compound-compound target and compound target-EMS target networks, key targets were analyzed for pathway enrichment. MMP-TIMP were uncovered as one cluster of the core targets. Furthermore, autologous transplantation of EMS rat's model were used to evaluate in vivo effect of JFS on invasion, metastasis and epithelial-mesenchymal transition. JFS significantly suppressed the growth, and reduced the volume of ectopic endometrium, with modification of pathologic structure. In-depth study, invasion and metastasis were restrained after treating with JFS through decreasing MMP-2 and MMP-9, increasing TIMP-1. Meanwhile, JFS promoted E-cadherin, and attenuated N-cadherin, Vimentin, Snail, Slug, ZEB1, ZEB2, Twist. In brief, anti-EMS effect of JFS might be related to the regulation of epithelial-mesenchymal transformation, thereby inhibition of invasion and metastasis. These findings reveal the potential mechanism of JFS on EMS and the benefit for further evaluation.
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Project description:We report the use of transcriptome sequencing in the intervention of luteolin or quercetin in adipogenesis. We constructed the adipogenic differentiation model of mouse embryonic fibroblasts and obtained the differential genes of luteolin or quercetin regulating adipocyte differentiation by transcriptomic sequencing. We identified 2085 differentially expressed lipogenesis response genes, 181 luteolin response genes and 574 quercetin response genes. This study provides a framework for the network regulation mechanism of luteolin or quercetin inhibiting preadipocyte differentiation.
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Project description:We performed gene expression analysis human peritoneal endometriosis lesions, eutopic endometrium from endometriosis patients and peritoneum form endometriosis patients.The goal of the study was to analyse gene expression differences between peritoneal endometriosis lesion and eutopic endometrium and peritoneal endometriosis lesion and peritoneum.
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