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Taohong Siwu Decoction relieves renal fibrosis: based on network pharmacology and experimental confirmation
Xiao-Qian Zhang1, Yi Gong1, Yi-Han Wang1
1Department of Nephrology, The Affiliated Traditional Medicine Hospital, Southwest Medical University, Luzhou, China.
Background:
Renal fibrosis is a critical process in chronic kidney disease (CKD) that can progress to end-stage renal disease (ESRD). Taohong Siwu Decoction (THSWD) has shown potential for anti-fibrotic effects, but its underlying mechanisms remain unclear.
Objective:
To investigate the anti-fibrotic mechanisms of THSWD using network pharmacology and cellular validation.
Methods:
Active components and targets of THSWD were identified. Analyses of drug-component-target networks and protein interactions were conducted. Functional enrichment and molecular docking assays were performed. Western blotting was used to evaluate epithelial-mesenchymal transition (EMT) markers (E-cadherin, Twist, N-cadherin, Vimentin, α-SMA, Fibronectin) and proteins in the Phosphoinositide 3-Kinase (PI3K)/Protein Kinase B (AKT)/Glycogen Synthase Kinase-3β (GSK-3β) pathway in TGF-β-stimulated TCMK1 cells.
Results:
THSWD comprises 61 active components and 213 targets, 59 of which overlap with renal fibrosis targets. Enrichment analyses highlighted the IL-11 and PI3K/AKT pathways. Molecular docking identified β-sitosterol as a key component. In TGF-β-stimulated cells, β-sitosterol (5-20μmol·L-1) upregulated E-cadherin and Twist in a dose-dependent manner and suppressed mesenchymal markers (Vimentin, N-cadherin, α-SMA, Fibronectin) and PI3K/AKT/GSK-3β phosphorylation.
Conclusion:
THSWD, primarily through β-sitosterol, alleviates renal fibrosis by modulating the PI3K/AKT/GSK-3β signaling pathway and EMT process (via E-cadherin and Twist), offering a novel therapeutic strategy for CKD.
