ArticleIranian journal of basic medical sciences2026
Cinnamophilin ameliorates testosterone-induced prostatic hyperplasia and fibrosis by regulating 5α-reductase and TGF-β/Smad signaling pathway.
Article in Iranian journal of basic medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objectives: Androgen and TGF-β1/Smad signaling pathways play important roles in epithelial-mesenchymal transition (EMT), fibrosis, and the development of benign prostatic hyperplasia (BPH). Cinnamophilin is extracted from Materials and Methods: The study was conducted both Results: Cinnamophilin (40 mg/kg) significantly reduced prostate weight and prostate index in animal models. Cinnamophilin inhibited the protein expression of 5α-reductase type II and prostate-specific antigen (PSA) in TP-treated mice. Cinnamophilin reversed morphological changes, EMT, and fibrosis in TP-treated mice. Cinnamophilin increased E-cadherin but decreased N-cadherin, vimentin, fibronectin, α-SMA, TGFBR2, TGF-β1, p-Smad2/3, collagen I, collagen III, and collagen IV protein expressions. The expression of Smad2/3 was not significantly different among these groups. Cinnamophilin (100 μM) inhibited proliferation at 48 hr in BPH-1 and WPMY-1 cells. Conclusion: These findings suggest that cinnamophilin inhibits prostate growth and mitigates EMT and fibrosis by regulating TGFβ/Smad signaling pathways.
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