Evidence map›Paper›PMID 39705287›Full record

ArticlePloS one2024

Integrating network pharmacology and experimental validation to explore the pharmacological mechanism of Astragaloside IV in alleviating urotensin II-mediated renal tubular epithelial cell injury.

Wenyuan Liu, Qianwei Liu, Ziyuan Zhang, Yaling Hu, Jingai Fang

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Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Wenyuan LiuDepartment of Nephrology, The First Hospital, Shanxi Medical University, Taiyuan, Shanxi, China.
Qianwei LiuShanxi Medical University, Taiyuan, Shanxi, China.
Ziyuan ZhangDepartment of Nephrology, The First Hospital, Shanxi Medical University, Taiyuan, Shanxi, China.
Yaling HuDepartment of Nephrology, The First Hospital, Shanxi Medical University, Taiyuan, Shanxi, China.
Jingai FangDepartment of Nephrology, The First Hospital, Shanxi Medical University, Taiyuan, Shanxi, China.ORCID 0009-0002-2084-8781

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal tubular epithelial cell injury is an important manifestation of chronic kidney disease (CKD). This study aims to explore the mechanism of astragaloside IV (AS-IV) in the treatment of UII-mediated renal tubular epithelial cell injury by integrating network pharmacology and experimental validation. BATMAN, SwissTarget-Prediction and ETCM data bases were used to screen the target proteins of AS-IV. DAVID software was then used to perform GO and KEGG enrichment analysis on these target genes, and STRING and cytoscape were used to construct a protein interaction network. Molecular docking analysis was performed on key genes. The CCK8 assay was applied to detect the cell viability. ELISA, laser confocal, RT-PCR, and Western blot methods were used to detect the expression of cell pathway indicators and inflammatory factors in each group. Network pharmacology analysis found that the cAMP signaling pathway is one of the most important pathways for AS-IV to treat CKD. Molecular docking results showed that the AS-IV can be well embedded in the active pockets of target proteins, such as ALB, VEGFA, AKT1, ROCK1, and DRD2. The cAMP content and expression of GPR-14, PKA, NF-κB, and TGF-β in the UII group and the UII+cAMP agonist group (Forskolin) were all higher than those in the control group (P<0.05). In the UII+SB-611812 group, UII+AS-IV group, UII+losartan group, and UII+cAMP inhibitor (H89) group, the cAMP content and the expressions of GPR-14, PKA, NF-κB and TGF-β were all decreased compared with those in the UII group (P<0.05). In conclusion, AS-IV may improve UII-mediated renal tubular epithelial cell damage by down-regulating the cAMP/PKA signaling pathway.

Indexed as

Epithelial CellsKidney TubulesMolecular Docking SimulationNetwork PharmacologySaponinsSignal TransductionTriterpenesUrotensinsCell LineCell SurvivalCyclic AMPHumansProtein Interaction Mapsastragaloside ACyclic AMPSaponinsTriterpenesurotensin IIUrotensins

Identifiers

PMID39705287
PMCPMC11661590

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.