ArticleEvidence-based complementary and alternative medicine : eCAM2022
Network Pharmacology and In Vivo Experimental Validation to Uncover the Renoprotective Mechanisms of Fangji Huangqi Decoction on Nephrotic Syndrome.
Article in Evidence-based complementary and alternative medicine : eCAM, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Programmed Cell Death: A Key Mechanism of Traditional Chinese Medicine in the Treatment of Membranous Nephropathy.Drug design, development and therapy · 2026Review
- Deciphering cellular heterogeneity and pathway dynamics in urinary samples: a UMAP-Based approach to understanding acute kidney injury.Frontiers in pharmacology · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
Background: Fangji Huangqi decoction (FHD) is a traditional Chinese medicine formula that has the potential efficacy for nephrotic syndrome (NS) treatment. This study aims to explore the effects and underlying mechanisms of FHD against NS via network pharmacology and in vivo experiments. Methods: The bioactive compounds and targets of FHD were retrieved from the TCMSP database. NS-related targets were collected from GeneCards and DisGeNET databases. The compound-target and protein-protein interaction networks were constructed by Cytoscape 3.8 and BisoGenet, respectively. GO and KEGG analyses were performed by the DAVID online tool. The interactions between active compounds and hub genes were revealed by molecular docking. An NS rat model was established to validate the renoprotective effects and molecular mechanisms of FHD against NS in vivo. Results: A total of 32 hub genes were predicted to play essential roles in FHD treating NS. Eight main bioactive compounds of FHD had the good affinity with 9 hub targets (CCL2, IL-10, PTGS2, TNF, MAPK1, IL-6, CXCL8, TP53, and VEGFA). The therapeutic effect of FHD on NS was closely involved in the regulation of inflammation and PI3K-Akt pathway. In vivo experiments confirmed the renoprotective effect of FHD on NS, evidenced by reducing the levels of proteinuria, serum creatinine, blood urea nitrogen, and inflammatory factors in NS rats. The PI3K activator 740Y-P weakened the effects of FHD against NS. Furthermore, FHD downregulated the levels of PTGS2, MAPK1, IL-6, and p-Akt in NS rats. Conclusions: FHD alleviates kidney injury and inflammation in NS by targeting PTGS2, MAPK1, IL-6, and PI3K-Akt pathway.
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