AI Summary & Key Takeaways
AI InsightConclusion: The results of the present study demonstrated that EGCG represses pp-38 and NF-kB signaling pathways, exerting a protective effect for scleroderma through its anti-oxidative role.
📌 3 Key Takeaways
Özet
Objectives: This study aims to evaluate the antioxidant effects of epigallocatechin-3-gallate (EGCG) in a bleomycin (BLM)-induced scleroderma model. Materials and methods: Thirty-two healthy female Balb-c mice (6-8-week-old; weighing 22±5 g) were used in this study. The mice were randomly divided into four groups: control (n=8), BLM (n=8), BLM+EGCG (n=8), and EGCG (n=8). Skin tissue specimens were collected at the end of the experiments. Histopathological examinations of skin tissues were performed. Skin samples were assessed for total superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. The phosphorylation of p-38 mitogen-activated protein kinase and Akt protein (the serine-threonine protein kinase encoded by the AKT), as well as the nuclear factor-kappa B (NF-kB) levels, were analyzed by western blotting. Results: Epigallocatechin-3-gallate-treated groups were observed to have reduced connective tissue fibrosis in the dermis area using Masson’s trichrome staining method. Pp-38 and NF-kB were found to decrease significantly in the BLM + EGCG group compared with the BLM group. Parallel to these findings, phosphorylated Akt protein was found to increase in the BLM + EGCG group compared with the BLM group. SOD activity was increased in the EGCG group and content of MDA level was decreased in EGCG groups. Conclusion: The results of the present study demonstrated that EGCG represses pp-38 and NF-kB signaling pathways, exerting a protective effect for scleroderma through its anti-oxidative role.