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Métodos Terapéuticos y Terapias MTCI
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1.
J Pharm Pharm Sci ; 26: 11234, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-36942296

RESUMEN

Background: Polycystic ovarian syndrome (PCOS) is the most common endocrine disorder affecting women. Chinese herbs have been considered as an alternative treatment for PCOS, and Yi-mu-cao (Leonuri Herba) is one of the most commonly used herbs to treat PCOS, which can relieve symptoms of PCOS patients. But the mechanism of its treatment remains unclear. Method: The main active ingredients and potential targets of Leonuri Herba were obtained by TCMSP and Swiss Target Forecast, and the related targets of PCOS were obtained by searching DrugBank, GeneCard and DisGeNet databases. The Protein-Protein Interaction (PPI) network was constructed using STRING database. GO and KEGG were used to detect the enrichment pathways of key targets. Cytoscape software was used to construct the component-target-pathway network, analyze the PPI network core, and verify the reliability of target binding by molecular docking technology. Result: 8 components and 116 targets of Leonuri Herba on PCOS were screened. Common targets mainly involve the Lipid and atherosclerosis, Endocrine resistance, AGE-RAGE signaling in diabetic complications and other signaling pathways. It is suggested that it can form multi-target and multi-pathway regulatory network through quercetin, kaempferol and other active substances to regulate endocrine disorders and reduce inflammatory response, so as to systematically improve PCOS. Molecular docking experiments showed that the active constituents of Leonurus had good binding activity with potential targets of PCOS. Conclusion: In summary, this study elucidates the potential effect of Leonuri Herba on PCOS, which is helpful to provide reference for clinical practice. This is also conducive to the secondary development of motherwort and its monomer components, and precision medicine for PCOS.


Asunto(s)
Aterosclerosis , Medicamentos Herbarios Chinos , Síndrome del Ovario Poliquístico , Humanos , Femenino , Síndrome del Ovario Poliquístico/tratamiento farmacológico , Simulación del Acoplamiento Molecular , Farmacología en Red , Reproducibilidad de los Resultados , Medicamentos Herbarios Chinos/farmacología , Medicamentos Herbarios Chinos/uso terapéutico , Medicina Tradicional China
2.
J Reprod Immunol ; 153: 103666, 2022 09.
Artículo en Inglés | MEDLINE | ID: mdl-35970081

RESUMEN

Recurrent spontaneous abortion (RSA) is a disturbing pregnancy disorder experienced by ~2.5% of women attempting to conceive. The pathogenesis of RSA is still unclear. Previous findings revealed that transcription factor YIN-YANG 1(YY1) was related to the pathogenesis of RSA by influence trophoblastic cell invasion ability. Present study aimed to investigate more specific molecular mechanism of YY1 playing in trophoblastic cells. In our research, RNA-seq and Chip-seq were used to find significant changed genes between si-YY1(Knock down of YY1) HTR-8/SVneo cells(n = 3) and HTR-8/SVneo cells(n = 3). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis results suggested that Integrins related pathway maybe necessary to biological functions of trophoblastic cells. Chip-seq dataset analysis results predict YY1 can regulate ITGA3/7 expression by binding to the promoter region of ITGA3/7. Furthermore, results from chip experiment, RT-PCR, Dual-luciferase reporter gene assay showed that YY1 was able to bind to the promoter region of ITGA3 and regulate ITGA3 mRNA and protein expression. However, ITGA7 could not be significant influenced by YY1. Besides, gene silencing experiment, Western blot and Immunofluorescence assay confirmed that both YY1 and ITGA3 can accelerate phosphorylation focal adhesion kinase and affect cytoskeleton formation in HTR-8/SVneo cells. In conclusion, YY1/ITGA3 play a critical role in trophoblast invasion ability by regulating cytoskeleton formation.


Asunto(s)
Aborto Habitual , Citoesqueleto , Integrina alfa3 , Trofoblastos , Factor de Transcripción YY1 , Aborto Habitual/genética , Aborto Habitual/metabolismo , Aborto Habitual/patología , Movimiento Celular/genética , Proliferación Celular/genética , Citoesqueleto/genética , Citoesqueleto/metabolismo , Femenino , Proteína-Tirosina Quinasas de Adhesión Focal/metabolismo , Humanos , Integrina alfa3/genética , Integrina alfa3/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Embarazo , ARN Mensajero/metabolismo , Trofoblastos/metabolismo , Factor de Transcripción YY1/genética , Factor de Transcripción YY1/metabolismo
3.
J Cell Physiol ; 235(10): 6637-6646, 2020 10.
Artículo en Inglés | MEDLINE | ID: mdl-32003019

RESUMEN

Insufficient trophoblast invasion is the key factor for the occurrence of recurrent spontaneous abortions (RSA). Our previous studies identified Yin Yang 1 (YY1) as a transcription factor involved in the regulation of trophoblast invasiveness at the maternal-fetal interface. Long noncoding RNAs (lncRNAs) can regulate gene expression and autophagy in many ways. The purpose of this study was to explore the relationship between YY1 and lncRNAs and the mechanism by which lncRNAs affect the biological behavior of trophoblasts. Bioinformatic analysis predicted that YY1 had three binding sites in the plasmacytoma variant translocation 1 (PVT1) promoter region. Chromatin immunoprecipitation experiments and electrophoretic mobility shift assays verified that YY1 can directly bind to the PVT1 promoter. Compared with its expression levels in human placental villi tissue samples from the normal pregnancy group, the PVT1 expression levels were significantly lower in tissues from the RSA group. PVT1 knockdown significantly reduced adhesion, invasion, autophagy, and mTOR expression in HTR-8/SVneo cells and greatly increased apoptosis in vitro. This study revealed a novel regulatory pathway in which YY1 can act directly on PVT1 promoter to regulate its transcription, which further affects trophoblast invasion and adhesion by regulating autophagy via the mTOR pathway, and these effects might be involved in RSA pathogenesis.


Asunto(s)
Autofagia/genética , Adhesión Celular/genética , ARN Largo no Codificante/genética , Transducción de Señal/fisiología , Serina-Treonina Quinasas TOR/genética , Trofoblastos/fisiología , Factor de Transcripción YY1/genética , Aborto Habitual/genética , Adulto , Apoptosis/genética , Autofagia/fisiología , Adhesión Celular/fisiología , Línea Celular , Movimiento Celular/genética , Femenino , Regulación de la Expresión Génica/genética , Humanos , Embarazo , Regiones Promotoras Genéticas/genética , Transcripción Genética/genética , Adulto Joven
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