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Métodos Terapéuticos y Terapias MTCI
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1.
Chem Biodivers ; 18(1): e2000810, 2021 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-33251769

RESUMEN

Guchang Zhixie Wan (GZW) is a commonly used Chinese medicine for the treatment of ulcerative colitis (UC). This research explored the potential pharmacological mechanism of GZW in UC. The active ingredients, potential targets, and UC-related genes of GZW were retrieved from public databases. The pharmacological mechanisms including key components, potential targets and signal pathways were determined through bioinformatics analysis. The results of this study were verified through virtual molecular docking and cell experiments. Network analysis revealed that 26 active GZW compounds and 148 potential GZW target proteins were associated with UC. Quercetin, kaempferol and ß-sitosterol were identified as the core active ingredients of GZW. IFNG, IL-1A, IL-1B, JUN, RELA, and STAT1 were indicated as key targets of GZW. These key targets have a strong affinity for quercetin, kaempferol, and ß-sitosterol. GO and KEGG enrichment analysis showed that GZW target proteins are highly enriched in inflammatory, immune, and oxidative stress-related pathways. This study confirmed the therapeutic effect and revealed potential molecular mechanism of GZW on UC. And the protective effects of GZW on inflammatory bowel disease pathway were also revealed through STAT3/NF-κB/IL-6 pathway. The findings of this study enhanced our understanding of GZW in the treatment of UC and provided a feasible method for discovering potential drugs from traditional Chinese medicine formulations.


Asunto(s)
Medicamentos Herbarios Chinos/metabolismo , Animales , Sitios de Unión , Colitis Ulcerosa/tratamiento farmacológico , Colitis Ulcerosa/patología , Medicamentos Herbarios Chinos/química , Medicamentos Herbarios Chinos/farmacología , Medicamentos Herbarios Chinos/uso terapéutico , Humanos , Interleucina-6/sangre , Interleucina-6/metabolismo , Medicina Tradicional China , Ratones , Simulación del Acoplamiento Molecular , Mapas de Interacción de Proteínas , Células RAW 264.7 , Factor de Transcripción STAT3/sangre , Factor de Transcripción STAT3/metabolismo , Transducción de Señal/efectos de los fármacos , Factor de Transcripción ReIA/sangre , Factor de Transcripción ReIA/metabolismo
2.
Biosci Rep ; 39(1)2019 01 31.
Artículo en Inglés | MEDLINE | ID: mdl-30463907

RESUMEN

Large doses of flavonoids could cure many diseases with no serious side effects. However, the role of flavonoids in the treatment of polycystic ovary syndrome (PCOS) has not been reported. Therefore, total flavonoids extracted from Nervilia Fordii were selected to explore its therapeutic efficiency in PCOS. PCOS rat model was constructed to explore the role of total flavonoids in the treatment of PCOS. ELISA was used to assess the changes of ovulation function under the treatment of total flavonoids with or without exogenous interleukin-6 (IL-6). Western blot, real-time PCR and immunohistochemistry were carried out to assess the related molecular mechanisms. We explored that total flavonoids obviously increased the serum levels of follicle-stimulating hormone (FSH), and sharply decreased the serum levels of luteinizing hormone (LH), testosterone (T) and insulin (INS) in the PCOS-IR rats via partly inhibiting the activation of JAK2/STAT3 pathway, partially up-regulating the IL-6 expression and partially down-regulating the suppressor of cytokine signaling 3 (SOCS3) expression in ovaries of PCOS rats. The effect of total flavonoids on estrous cycles, serum levels of FSH, LH, T and INS were partially attenuated by IL-6 in PCOS rat model. Moreover, IL-6 significantly reversed the effect of total flavonoids on the phosphorylation of JAK2/STAT3, the expression of IL-6 and SOCS3 in ovaries of PCOS rats. Total flavonoids extracted from Nervilia Fordii might induce the expression of IL-6 in ovary and act as a potential therapeutic drug for the treatment of PCOS.


Asunto(s)
Antineoplásicos Fitogénicos/farmacología , Flavonoides/farmacología , Interleucina-6/genética , Janus Quinasa 2/genética , Orchidaceae/química , Síndrome del Ovario Poliquístico/tratamiento farmacológico , Factor de Transcripción STAT3/genética , Animales , Antineoplásicos Fitogénicos/aislamiento & purificación , Glucemia , Gonadotropina Coriónica/administración & dosificación , Modelos Animales de Enfermedad , Ciclo Estral/efectos de los fármacos , Femenino , Flavonoides/aislamiento & purificación , Hormona Folículo Estimulante/sangre , Hormona Folículo Estimulante/genética , Regulación Neoplásica de la Expresión Génica , Humanos , Insulina/administración & dosificación , Insulina/sangre , Resistencia a la Insulina , Interleucina-6/sangre , Interleucina-6/farmacología , Janus Quinasa 2/sangre , Hormona Luteinizante/sangre , Hormona Luteinizante/genética , Ovulación/efectos de los fármacos , Extractos Vegetales/química , Síndrome del Ovario Poliquístico/inducido químicamente , Síndrome del Ovario Poliquístico/genética , Síndrome del Ovario Poliquístico/patología , Ratas , Ratas Sprague-Dawley , Factor de Transcripción STAT3/sangre , Transducción de Señal , Testosterona/sangre , Testosterona/genética
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