Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Adicionar filtros








Intervalo de ano
1.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 11-18, 2023.
Artigo em Chinês | WPRIM | ID: wpr-998158

RESUMO

ObjectiveTo investigate the effects of Fangji Fulingtang on macrophage polarization and oxidative stress in the mouse model of myocardial fibrosis. MethodThe mouse model of myocardial fibrosis was established by subcutaneous injection of isoproterenol (ISO, 5 mg·kg-1·d-1). Fifty C57BL/6J mice were randomly assigned into control (0.9% NaCl), model (0.9% NaCl), low- and high-dose (3.315 g·kg-1·d-1 and 13.26 g·kg-1·d-1, respectively) Fangji Fulingtang (FFD-L and FFD-H, respectively), and metoprolol tartrate (Meto, 15 mg·kg-1·d-1) groups, with 10 mice each group. After 2 weeks of treatment, the heart appearance, cardiac weight index (CWI), heart weight (HW)/tibia length (TL) ratio, and myocardial histopathological alterations were observed. Meanwhile, the serum levels of creatine kinase-MB (CK-MB), transforming growth factor-β1 (TGF-β1), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-10, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were measured by enzyme-linked immunosorbent assay (ELISA). The expression levels of CD86 and CD206 were observed by immunohistochemical staining. ResultCompared with the model group, the FFD-L, FFD-H, and Meto groups showed improved heart appearance, decreased CWI and HW/TL ratio (P<0.01), lowered serum levels of CK-MB, TGF-β1, TNF-α, IL-1β, and IL-6 (P<0.05, P<0.01), and elevated IL-10 level (P<0.05). Furthermore, the three groups showed reduced infiltration of inflammatory cells, myocardial injury, collagen deposition, and myocardial fibrosis, decreased CD86, SOD, and GSH (P<0.01), and increased CD206 and MDA (P<0.01). ConclusionFangji Fulingtang can mitigate ISO-induced myocardial fibrosis by regulating macrophage polarization and oxidative stress.

2.
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 175-182, 2022.
Artigo em Chinês | WPRIM | ID: wpr-940401

RESUMO

ObjectiveTo explore the mechanism of Fangji Fulingtang in the treatment of acute kidney injury (AKI) induced by ischemia-reperfusion based on network pharmacology and experimental verification. MethodActive components of Fangji Fulingtang were retrieved from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and previous report and targets of these components were predicted by SwissTargetPrediction. The targets of AKI were searched from GeneCards, Online Mendelian Inheritance in Man (OMIM), the database of gene-disease associations (DisGeNET), and Therapeutic Target Database (TTD). Protein-protein interaction (PPI) network was constructed by STRING. Metascape was used for Gene Ontology (GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment of core targets. Cytoscape was employed to construct the "medicinal-active component-target-disease" network and “active component-target-pathway” network. AutoDock was applied for molecular docking. Finally, animal experiment was carried out to validate the mechanism of Fangji Fulingtang in treatment of AKI. ResultA total of 137 active components and 858 targets of Fangji Fulingtang, 1 294 targets of AKI, and 267 targets of Fangji Fulingtang in the treatment of AKI were screened out. Phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), proto-oncogene tyrosine protein kinase (SRC), protein kinase B1 (Akt1), and mitogen-activated protein kinase 3 (MAPK3) were the key anti-AKI targets of Fangji Fulingtang, which were involved in 1 609 GO terms, particularly cell response to lipids, membrane rafts, and protein kinase activity, and 140 KEGG pathways such as PI3K/Akt signaling pathway, chemokine signaling pathway, and Toll-like receptor signaling pathway. Molecular docking showed that the core active components had strong binding affinity to the key targets. The hematoxylin and eosin (HE) staining results indicated that Fangji Fulingtang can significantly improve the pathological state and the serological results suggested that the levels of serum creatinine (SCr) and blood urea nitrogen (BUN) were significantly reduced. ConclusionThis study clarified the mechanism of Fangji Fulingtang in the treatment of AKI and found that Fangji Fulingtang had the multi-component, multi-target, and multi-pathway characteristics in the treatment of AKI. The result lays a foundation for further study of its specific mechanism.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA