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基于Nrf2/HO-1信号通路研究梓醇改善真皮成纤维细胞氧化损伤的机制
Authors Lang X , Xu L, Li L, Feng X
Received 6 April 2024
Accepted for publication 8 June 2024
Published 18 June 2024 Volume 2024:18 Pages 2287—2297
DOI https://doi.org/10.2147/DDDT.S467569
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Anastasios Lymperopoulos
Xiaona Lang,1 Liyan Xu,2 Lu Li,1 Xin Feng1
1Pharmacy Department, Tianjin Hospital, Tianjin, People’s Republic of China; 2Orthopedic Department, Tianjin Hospital, Tianjin, People’s Republic of China
Correspondence: Xin Feng, Pharmacy Department, Tianjin Hospital, Tianjin, People’s Republic of China, Tel +86-13652001152, Email fx_yutong@126.com
Objective: Catalpol, as a natural medicine small-molecule drug, has been proven to have anti-inflammatory and antioxidant pharmacological effects.
Methods: The effect of catalpol on oxidative damage of mouse epidermal fibroblast L929 model and its mechanism were investigated by using hydrogen peroxide model, CCK8 method, flow cytometry, and Western blot.
Results: The effect of catalpol on Nrf2/HO-1 signaling pathway was further studied to improve oxidative stress in cell models. The results showed that catalpol had no cytotoxicity to L929 cells, and inhibited the apoptosis of L929 cells after oxidative damage in a concentration-dependent manner, thus playing a role in cell protection. The oxidative damage of cells was inhibited by up-regulating the expression of the signature protein of Nrf2/HO-1 signaling pathway and inhibiting the interstitial formation of cells.
Conclusion: This study is a preliminary study on the protective function of catalpol against oxidation and apoptosis in dermal fibroblasts, which can provide a theoretical basis and drug guidance for promoting skin wound healing in the later stage.
Keywords: catalpol, oxidative damage, Nrf2/HO-1, dermal fibroblasts, oxidative stress