Progress and Prospects of Research Ideas and Methods in the Network Pharmacology of Traditional Chinese Medicine

Yuan, Zhongzhu; Pan, Yingying; Leng, Tian; Chen, Yu; Zhang, Haojie; Ma, Jinjin; Ma, Xiaoju

doi:10.18433/jpps32911

Cited by 67 publications

(39 citation statements)

References 18 publications

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“…However, network pharmacology research is based on network modeling, database resource development and software application. 71 Thus, we further investigated the anti-inflammatory effects of compounds 1 , 2 , 3 and 4 in LPS-stimulated RAW 264.7 cell. The results show compounds 1 , 2 , 3 and 4 inhibited the production of NO and IL-6, and the expression of COX-2.…”

Section: Resultsmentioning

confidence: 99%

Isolation of oligostilbenes fromIris lacteaPall. var.chinensis(Fisch.) Koidz and their anti-inflammatory activities

Tie

et al. 2022

RSC Adv.

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Section: Resultsmentioning

confidence: 99%

Isolation of oligostilbenes fromIris lacteaPall. var.chinensis(Fisch.) Koidz and their anti-inflammatory activities

Tie

et al. 2022

RSC Adv.

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“…Network pharmacology utilizes a combination of artificial intelligence and medicine to facilitate biomedical research, analyze massive biomedical data, and establish transformation from data to knowledge. Network pharmacology has become a popular tool that is widely used in the elucidation of mechanisms in TCM pharmacology and screening of TCM active ingredients, drug repositioning, exploration of TCM compatibility mechanisms, and interpretation of the multicomponent, multitarget, and multipathway action mechanisms in TCM [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Tiao‐Bu‐Fei‐Shen Formula Improves Glucocorticoid Resistance of Chronic Obstructive Pulmonary Disease via Downregulating the PI3K‐Akt Signaling Pathway and Promoting GRα Expression

Zhou

et al. 2023

Evidence-Based Complementary and Alternative Medicine

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Objective. To predict and determine the mechanism through which Tiao-Bu-Fei-Shen (TBFS) formula improves glucocorticoid resistance in chronic obstructive pulmonary disease (COPD), using network pharmacology, molecular docking technology, and in vitro studies. Methods. The main active components and associated targets of TBFS were screened using the systems pharmacology database of traditional Chinese medicine database (TCMSP). The main COPD targets were retrieved from the Human Gene (GeneCards) and DrugBank databases. A protein-protein interaction (PPI) network was constructed using the protein interaction platform STRING and Cytoscape 3.6.1. Gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genome Pathway (KEGG) analyses were performed using the biological information annotation database Metascape. Molecular docking was performed using the AutoDock Vina software. THP-1 monocytes were treated with TBFS-containing serum and cigarette smoke extract (CSE) for 48 h, and cell proliferation in each group was determined using cell counting kit-8 (CCK-8). A COPD cell model was constructed by stimulating THP-1 monocytes with CSE for 12 h. A lentivirus vector for RNA interference of histone deacetylase 2 (HDAC2) gene was constructed and transfected into the THP-1 monocytes, and the transfection efficiency was verified using quantitative polymerase chain reaction (qPCR) and western blotting (WB). The expression of HDAC2 in each group of cells was detected using qPCR, and the expression of HDAC2, phosphoinositide-3 kinase (PI3K) p85α, glucocorticoid receptor α (GRα), and P-AKT1 in each group of cells was detected through WB. Results. A total of 344 TBFS active components, 249 related drug targets, 1,171 COPD target proteins, and 138 drug and disease intersection targets were obtained. Visual analysis of the PPI network map revealed that the core COPD targets of TBFS were AKT1, IL-6, TNF, TP53, and IL1-β. KEGG pathway enrichment analysis resulted in the identification of 20 signaling pathways as the main pathways involved in the action of TBFS against COPD, including the PI3K-Akt, TNF, and IL-17 signaling pathways. Molecular docking experiments revealed a strong binding capacity of kaempferol, luteolin, and quercetin to the ATK1 protein in TBFS, with quercetin performing the best. PCR results showed that treatment with TBFS significantly increased the expression levels of HDAC2 in the COPD model. WB results showed that TBFS treatment significantly increased the expression levels of GRα and HDAC2 in the COPD model, while reducing the expression levels of P-AKT1. Conclusion. TBFS treatment improves glucocorticoid resistance observed in COPD through downregulation of the PI3K-Akt signaling pathway and promotion of GRα expression.

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“…It is characterized by the “disease-phenotype-gene-drug” interaction network and focuses on the comprehensive and systematic study of the mechanism of drug intervention on the disease network, which coincides with the holistic view of TCM ( 47 ). The general process of network pharmacology research includes the following technical links: the collection of active ingredients, the collection of target groups of related diseases, the integration of disease targets and compound targets, network construction and gene enrichment analysis ( 48 , 49 ). Even though, network pharmacology has broken through the previous research pattern of single target and changed into the research model of “network target”, there are still many problems in its practical application, such as incomplete database information and the lack of experimental verification ( 50 ).…”

Section: Discussionmentioning

confidence: 99%

Yishen Xiezhuo formula ameliorates the development of cisplatin-induced acute kidney injury by attenuating renal tubular epithelial cell senescence

Zhang¹,

Qi²,

Luo³

et al. 2022

Ann Transl Med

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Background: Although cisplatin (DDP) is an important clinical anti-tumor drug, its use is limited by its nephrotoxicity. How to avoid the renal injury incurred by platinum drugs and improve the clinical efficiency of platinum drugs use has become an urgent clinical problem. Previous studies have verified that Chinese medicine has definite effects on acute kidney injury (AKI). Yishen Xiezhuo formula (YSXZ) is a traditional Chinese medicine (TCM) compound which is an effective clinical drug for AKI, but its mechanism remains unclear. Methods: In our research, an AKI model was induced by DDP in human renal tubular epithelial cell (HKC) lines in the in vitro study. The mechanism of the YSXZ on cell senescence was analyzed by Cell Counting Kit-8 (CCK-8), senescence-associated β-galactosidase (SA-β-Gal) staining, western blot, flow cytometry, and enzyme-linked immunosorbent assay (ELISA). Network pharmacology was used to analyze the role of YSXZ against AKI. Results: Compared with the control group, the cells in the DDP intervention group were significantly senescent. Compared with DDP group, YSXZ decreased the number of SA-β-Gal-positive senescence cells, down regulated the expression of senescence-related proteins, reduced the release of senescencerelated secreted phenotypic factors, and reversed the phenomenon of cell cycle S-phase arrest. Network pharmacology and experimental studies showed that the mitogen-activated protein kinase (MAPK) signaling pathway played a central role. Conclusions: Our present results suggested that YSXZ ameliorated the development of DDP-induced AKI by attenuating renal tubular epithelial cell (RTEC) senescence via alleviating the activation of MAPK pathway.

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Progress and Prospects of Research Ideas and Methods in the Network Pharmacology of Traditional Chinese Medicine

Cited by 67 publications

References 18 publications

Isolation of oligostilbenes fromIris lacteaPall. var.chinensis(Fisch.) Koidz and their anti-inflammatory activities

Isolation of oligostilbenes fromIris lacteaPall. var.chinensis(Fisch.) Koidz and their anti-inflammatory activities

Tiao‐Bu‐Fei‐Shen Formula Improves Glucocorticoid Resistance of Chronic Obstructive Pulmonary Disease via Downregulating the PI3K‐Akt Signaling Pathway and Promoting GRα Expression

Yishen Xiezhuo formula ameliorates the development of cisplatin-induced acute kidney injury by attenuating renal tubular epithelial cell senescence

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