Astaxanthin ameliorates benzalkonium chloride–induced dry eye disease through suppressing inflammation and oxidative stress via Keap1‐Nrf2/HO‐1 signaling pathways
AST is capable of shielding mice from BAC-induced DED, decelerating the progression of DED, and mitigating oxidative stress damage under HS conditions in hCEC cells. The protective impact of AST on DED may operate through stimulating the Keap1-Nrf2/HO-1 signaling pathway. Our research findings indicate that AST may be a promising treatment for DED, offering new insights into DED treatment.
Authors
- Jiayu Bao (ORCID: https://orcid.org/0000-0001-9476-3225)
- Jun Feng (ORCID: https://orcid.org/0000-0002-3695-1209)
- Ya Wen (ORCID: https://orcid.org/0009-0001-2339-5549)
- Peng Zhang (ORCID: https://orcid.org/0000-0003-4278-0036)
- Yinghui Wang (ORCID: https://orcid.org/0000-0002-8347-8194)
- Yaqiong Li (ORCID: https://orcid.org/0000-0001-9253-5878)
- Lei Tian (ORCID: https://orcid.org/0000-0002-7216-5352)
- Ying Jie (ORCID: https://orcid.org/0000-0003-2649-8241)
- Siyuan Li (ORCID: https://orcid.org/0000-0003-0617-2279)
- Ziyu Liu (ORCID: https://orcid.org/0000-0003-3890-5430)
Institutions
- Beijing Tongren Hospital (CN)
- Capital Medical University (CN)
Publication Details
- Journal
- Animal Models and Experimental Medicine
- Published
- 2025-03-05
- DOI
- https://doi.org/10.1002/ame2.70000
- Citations
- 5
- Primary Topic
- Ocular Surface and Contact Lens
- Type
- article
- Field-Weighted Citation Impact
- 9.39