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Data · dataset · 2026

Based on network pharmacology and experimental verification, the mechanism of Huangqi Jiaogenin in treating diabetic nephropathy is explored

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Description

Establishment of DN mouse model induced by high-fat diet combined with low-dose streptozotocin; By detecting fasting blood glucose, renal function related indicators, evaluating renal histopathology, and measuring oxidative stress and inflammatory response related indicators, the renal protective effect of AS-IV is assessed; Network pharmacology screening integrates common targets of AS-IV and DN, and conducts GO and KEGG enrichment analysis to screen key signaling pathways.

Molecular docking of key targets was performed using AutoDock Vina software and validated by Western blot. The results showed that AS-IV can significantly reduce fasting blood glucose, improve renal function, and alleviate renal tissue pathological damage in DN mice; Reduce the levels of tumor necrosis factor - α, interleukin-6, IL-1 β, and malondialdehyde, increase the activity of superoxide dismutase and reduced glutathione, and inhibit the expression of alpha smooth muscle actin in renal tissue.

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Network pharmacology suggests that AS-IV mainly acts on key targets such as AKT serine/threonine kinase 1, mammalian rapamycin target protein, tumor necrosis factor, and caspase-3, significantly enriched in the phosphatidylinositol 3-kinase/protein kinase B/mTOR signaling pathway. Molecular docking shows that AS-IV has good binding ability with PI3K, AKT, and mTOR; Western blot results further confirmed that AS-IV significantly inhibited the expression levels of PI3K, p-AKT, and p-mTOR proteins in the kidney tissue of DN mice.

In summary, AS-IV may exert a renal protective effect by blocking the abnormal activation of the PI3K/AKT/mTOR signaling pathway, reducing oxidative stress and inflammatory response, improving renal function, and delaying the progression of renal fibrosis. 

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ScienceDB10.57760/sciencedb.nprd.002869 d agoJSON v1
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