ArticleFunctional & integrative genomics2023
Danggui Shaoyaosan attenuates doxorubicin induced Nephrotic Syndrome through regulating on PI3K/Akt Pathway.
Article in Functional & integrative genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Correlation of Oxidative Stress Biomarkers with Activity of Pediatric Idiopathic Nephrotic Syndrome.Biomedicines · 2025Article
- Calycosin ameliorates albuminuria in nephrotic syndrome by targeting Notch1/Snail pathway.BMC nephrology · 2025Article
- Article
- Network Pharmacology and Molecular Docking Validation to Explore the Pharmacological Mechanism of Zhuling Decoction against Nephrotic Syndrome.Current pharmaceutical design · 2024Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The study aimed to explore the role and the underlying mechanism of Danggui Shaoyaosan (DSS) in nephrotic syndrome (NS). NS rat model was induced by doxorubicin injection twice. After DSS treatment, inflammation and oxidative stress index were detected via ELISA. Western blot was used for the protein detection. Go and KEGG analysis was applied to evaluate target gene and signaling of DSS. MCP-5 cell was applied for the cell rescue experiments and mechanism exploration. The 24 h urine protein levels of NS rats increased significantly, which was reduced by DSS treatment in a concentration-dependent manner. After DSS treatment, levels of BUN, SCr, TG and TC were also decreased, and serum ALB and TP levels were increased in rats. GO and KEGG pathway enrichment identified PI3K-Akt to be the candidate signaling of DSS in the treatment of NS, which was activated in NS rats. The recuse experiments in MCP-5 demonstrated that IGF-1, the agonist of PI3K/AKT, abolished the beneficial role of DSS in podocyte cell viability, apoptosis, inflammation and oxidative stress. In conclusion, DSS exerts a protective role against the development of NS. The mechanism is related to the improvement of podocyte injury and the inhibition of PI3K/Akt pathway-related proteins.
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Registered trials
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