ArticleBMC complementary medicine and therapies2020
Buyang Huanwu Tang inhibits cellular epithelial-to-mesenchymal transition by inhibiting TGF-β1 activation of PI3K/Akt signaling pathway in pulmonary fibrosis model in vitro.
Article in BMC complementary medicine and therapies, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 32 citations in OpenAlex.
- Inhibitory Mechanism of Buyang Huanwu Decoction on AGE/RAGE Pathway in Membranous Nephropathy: Integration of Network Pharmacology and Cell Model Validation.International journal of general medicine · 2026Article
- Current Understanding of Pulmonary Fibrosis: Pathogenesis, Diagnosis, and Therapeutic Approaches.Canadian respiratory journal · 2025Review
- Pinostilbene inhibits lung epithelial-mesenchymal transition and delays pulmonary fibrosis by modulating the PI3K/Akt pathway.Frontiers in pharmacology · 2025Article
- Yi-Fei-Tong-Bi Decoction Alleviates Bleomycin Induced Pulmonary Fibrosis in Mice.Drug design, development and therapy · 2025Article
- Article
- Traditional Chinese medicine inspired dual-drugs loaded inhalable nano-therapeutics alleviated idiopathic pulmonary fibrosis by targeting early inflammation and late fibrosis.Journal of nanobiotechnology · 2024Article
- Exploring the role and mechanism of Astragalus membranaceus and radix paeoniae rubra in idiopathic pulmonary fibrosis through network pharmacology and experimental validation.Scientific reports · 2023Article
- From Basic Research to Clinical Practice: Considerations for Treatment Drugs for Silicosis.International journal of molecular sciences · 2023Review
- Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis.Molecules (Basel, Switzerland) · 2022Review
- Therapeutic Effect of Astragali Radix Extract Injection Combined with Bone Marrow Mesenchymal Stem Cells in Bleomycin-Induced Pulmonary Fibrotic Rats.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Epithelial-mesenchymal transition in organ fibrosis development: current understanding and treatment strategies.Burns & trauma · 2022Review
- Protective Effects of the Wenfei Buqi Tongluo Formula on the Inflammation in Idiopathic Pulmonary Fibrosis through Inhibiting the TLR4/MyD88/NF-BioMed research international · 2022Article
- Buyang Huanwu Decoction protects against STZ-induced diabetic nephropathy by inhibiting TGF-β/Smad3 signaling-mediated renal fibrosis and inflammation.Chinese medicine · 2021Article
- Pterostilbene alleviates pulmonary fibrosis by regulating ASIC2.Chinese medicine · 2021Article
- MicroRNAs in Transforming Growth Factor-Beta Signaling Pathway Associated With Fibrosis Involving Different Systems of the Human Body.Frontiers in molecular biosciences · 2021Review
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5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPulmonary fibrosis (PF) is a chronic and progressive interstitial lung disease. Buyang Huanwu Tang (BYHWT), a classical traditional Chinese medicine formula, has been widely utilized for the treatment of PF in China. This present study aimed to explore the mechanism of BYHWT in the treatment of PF in vitro.
methodsTGF-β1 stimulated human alveolar epithelial A549 cells were used as in vitro model for PF. Post the treatment of BYHWT, cell viability was measured by MTT assay, and cell morphology was observed under microscope. The epithelial-to-mesenchymal transition (EMT) markers (E-cadherin, Vimentin) and collagen I (Col I) were detected by western blot, immunofluorescence staining and real-time quantitative polymerase chain reaction. With the co-administration of activators (IGF-1, SC79) and inhibitors (LY294002, MK2206), the effect of BYHWT on PI3K/Akt pathway was analyzed by western blot.
resultsBYHWT inhibited cell growth, and prevented cell morphology changed from epithelial to fibroblasts in TGF-β1 induced A549 cells. BYHWT decreased Vimentin and Col I, while increased E-cadherin at both protein and mRNA levels. Moreover, phosphorylation of PI3K (p-PI3K) and phosphorylation of Akt (p-Akt) were significantly down-regulated by BYHWT in TGF-β1 stimulated A549 cells.
conclusionThese results indicate that BYHWT suppressed TGF-β1-induced collagen accumulation and EMT of A549 cells by inhibiting the PI3K/Akt signaling pathway. These findings suggest that BYHWT may have potential for the treatment of PF.
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