The Mechanism of Catalpol to Improve Oxidative Damage of Dermal Fibroblasts Based on Nrf2/HO-1 Signaling Pathway

Abstract

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

Data Sharing Statement

All the data in the article are obtained by the authors themselves, and the pictures are also drawn by themselves. So no reference to any data set, all original. Six samples were prepared for each data, and the repeated experiment of each sample was carried out as a separate and independent experiment.

Ethical Approval

No ethical approval is required for this article.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare that the research was conducted without any commercial or financial relationships construed as a potential conflict of interest.

Additional information

Funding

This research was sponsored by Tianjin Health Research Project (TJWJ2023QN053).