Scholarlink

Background <p>Dry eye disease (DED) is a multifactorial ocular condition involving tear film instability, oxidative stress, and inflammation. This study investigated the therapeutic potential of XanMax® 2002, a lutein- and zeaxanthin-rich supplement, in a desiccating stress–induced DED mouse model and Pam3CSK4-stimulated human corneal epithelial cell line (HCE-2).</p> Methods <p>Oral administration of XanMax® 2002 for 14&#xa0;days was evaluated in DED mice for tear secretion, tear film stability, corneal damage, and ocular tissue integrity. Histological and biochemical analyses were conducted to measure oxidative (malondialdehyde (MDA), reactive oxygen species (ROS)) and inflammatory markers (IFN-γ, IL-1β, IL-6, TNF-α). In vitro, Pam3CSK4-stimulated HCE-2 cells were used to assess Toll-like receptor 2 (TLR2)-mediated proinflammatory gene expression and cytotoxicity.</p> Results <p>Oral administration of XanMax® 2002 significantly improved tear secretion and tear film stability, while reducing corneal damage and preserving ocular tissue structure. The supplement decreased oxidative and inflammatory markers in both serum and ocular tissues. In vitro, XanMax® 2002 suppressed TLR2-mediated expression of TNF-α, IL-6, IL-1β, and CCL-2 without inducing cytotoxicity. These effects were dose-dependent and comparable to those of cyclosporine A.</p> Conclusion <p>XanMax® 2002 confers ocular surface protection through dual modulation of oxidative and inflammatory responses and may represent a promising nutritional strategy for DED management.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Protective effects of XanMax® 2002 on ocular surface damage in dry eye disease: evidence from animal and cell models

  • 期刊论文

  • 发表日期：

    2025年10月26日

查看全文
  • Seohan Kim,
  • M. K. Priya,
  • Jinhak Kim,
  • Yuri Gwon,
  • Wonchul Lim,
  • Tae-Gyu Lim

摘要

Background

Dry eye disease (DED) is a multifactorial ocular condition involving tear film instability, oxidative stress, and inflammation. This study investigated the therapeutic potential of XanMax® 2002, a lutein- and zeaxanthin-rich supplement, in a desiccating stress–induced DED mouse model and Pam3CSK4-stimulated human corneal epithelial cell line (HCE-2).

Methods

Oral administration of XanMax® 2002 for 14 days was evaluated in DED mice for tear secretion, tear film stability, corneal damage, and ocular tissue integrity. Histological and biochemical analyses were conducted to measure oxidative (malondialdehyde (MDA), reactive oxygen species (ROS)) and inflammatory markers (IFN-γ, IL-1β, IL-6, TNF-α). In vitro, Pam3CSK4-stimulated HCE-2 cells were used to assess Toll-like receptor 2 (TLR2)-mediated proinflammatory gene expression and cytotoxicity.

Results

Oral administration of XanMax® 2002 significantly improved tear secretion and tear film stability, while reducing corneal damage and preserving ocular tissue structure. The supplement decreased oxidative and inflammatory markers in both serum and ocular tissues. In vitro, XanMax® 2002 suppressed TLR2-mediated expression of TNF-α, IL-6, IL-1β, and CCL-2 without inducing cytotoxicity. These effects were dose-dependent and comparable to those of cyclosporine A.

Conclusion

XanMax® 2002 confers ocular surface protection through dual modulation of oxidative and inflammatory responses and may represent a promising nutritional strategy for DED management.