ArticleFrontiers in pharmacology2025
Qinggan Yipi capsule ameliorates hepatic fibrosis in rats by down-regulating the TGF-β1/Smad2/3 signaling pathway and improving gut microbiota imbalance.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Therapeutic target exploration of Shugan Jianpi formula in liver fibrosis: an integrated lncRNA-mRNA co-expression network analysis.Molecular genetics and genomics : MGG · 2026Article
- The role of Traditional Chinese Medicine in the management of liver disease: targeting gut microbiome.Chinese medicine · 2026Review
- Mechanism of liver fibrosis induced by life-long triclosan exposure in offspring rats: an adverse outcome pathway framework validated by in vivo and in vitro experiments.Archives of toxicology · 2026Article
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7 authors.
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Abstract
Background and objective: Qinggan Yipi Capsule (QgYp) is a hospital preparation that has been used for many years in the treatment of chronic liver diseases. However, the mechanism of QgYp in ameliorating hepatic fibrosis (HF) remains unclear. This study aims to clarify the anti-liver fibrosis effect of QgYp and its mechanism of action. Methods: This study uses a carbon tetrachloride (CCl Results: Histopathological analysis, serum biochemical tests, and ELISA measurements showed that QgYp effectively decreased the levels of ALT, AST, HA, LN, PCIII, and IV-C while improving collagen deposition and hepatocyte necrosis. Protein-protein interaction (PPI) network analysis screened HF-related genes, including peroxisome proliferator-activated receptor gamma (PPARG), tumor necrosis factor (TNF), and TGF-β1. GO and KEGG analyses indicated that QgYp significantly affects TGF-β signaling pathway. In addition, the results of qPCR and Western blot analysis from both Conclusion: QgYp could effectively ameliorate HF, and this effect might be connected to the downregulation of the TGF-β1/Smad2/3 pathway, the suppression of HSCs activation, and regulation of gut microbiota dysbiosis.
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