Kocak, AyseHarmancı, DuyguBirlik, MerihSarioglu, SulenYilmaz, OsmanCavdar, ZahideAkdoğan, Gül2023-06-162023-06-1620180250-46851303-829Xhttps://doi.org/10.1515/tjb-2017-0185https://search.trdizin.gov.tr/yayin/detay/309413https://hdl.handle.net/20.500.14365/2318Objective: The aim of the present study was to evaluate the potential protective effects of epigallocatechin-3-gallate (EGCG) on fibrosis in bleomycin induced scleroderma model. Materials and methods: Thirty-two healthy female Balb-c mice with the average body weight of 22 +/- 5 g were used in this study. The mice were randomly divided into four groups as control (n=8), Bleomycin (n=8), Bleomycin+ EGCG (n =8) and EGCG (n =8). Skin tissue samples were collected to quantify matrix metalloproteinases (MMP-1, MMP-8, MMP-13), p-SMAD 2/3 and SMAD 2/3 in protein homogenates by western blotting. TGF-beta 1 expression was determined by real-time PCR. Immunohistopathological and histopathological examinations of skin tissues were also done. Results: When measured with Masson Trichrome, EGCG treatment was found to decrease fibrosis in connective tissue compared to the BLM injected control. EGCG was decreased dermal fibrosis. Bleomycin + EGCG group showed a significant reduction in fibrosis at the dermal surface area using hematoxylin measurements compared with the BLM group. MMP-1, MMP-8 protein levels were increased and p-SMAD 2/3 protein level was decreased. TGF-beta mRNA expression was decreased in the EGCG + BLM group compared with the BLM group. Conclusion: These results suggest an antifibrotic role for EGCG.eninfo:eu-repo/semantics/openAccessBLM induced SclerodermaEGCGFibrosisTGF-betaMMPsBleomycin-Induced SclerodermaReal-Time PcrSystemic-SclerosisAnimal-ModelGreen TeaGrowth-FactorCollagen ProductionSkin FibroblastsHepatic-FibrosisGene-ExpressionArticle10.1515/tjb-2017-01852-s2.0-85042011483