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Glucosamine mitigates hyperglycemic-induced oxidative stress via the SIRT1 pathway in human corneal epithelial cells

Yung-Yu Yang1, Shu-Ting Liu2, Shih-Ming Huang2

  • 1Department of Ophthalmology, Tri-Service General Hospital, National Defense Medical University, Taipei City 114, Taipei , Taiwan, Republic of China.

Scientific Reports
|October 14, 2025
PubMed

Insights

Glucosamine (GlcN) shows potential in protecting the corneal epithelium from high glucose (HG) damage by reducing oxidative stress and senescence, despite some cytotoxicity. Further research may lead to new therapies for diabetic vision complications.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Biochemistry

Background:

  • Hyperglycemia causes irreversible damage to the corneal epithelium, threatening vision.
  • High glucose (HG) levels induce oxidative stress and cellular senescence in corneal cells.
  • Developing therapeutic strategies to protect the corneal epithelium is crucial for preventing vision loss in diabetic patients.

Purpose of the Study:

  • To investigate the potential of glucosamine (GlcN) in counteracting the detrimental effects of high glucose (HG) on human corneal epithelial (HCE-T) cells.
  • To explore the molecular mechanisms by which GlcN affects cellular processes related to hyperglycemia-induced damage.
  • To assess GlcN's impact on oxidative stress, cellular senescence, cell cycle, and key protein expressions in HCE-T cells.

Main Methods:

  • Human corneal epithelial (HCE-T) cells were treated with high glucose (HG) and/or glucosamine (GlcN).
  • Cellular viability, reactive oxygen species (ROS) generation, and cell cycle distribution were analyzed.
  • Protein levels of KLF4, SIRT1, fibronectin, and claudin-1 were assessed using Western blotting.
  • The effects of SIRT1 inhibitors (Ex-527, INZ) on GlcN-treated cells were evaluated.

Main Results:

  • GlcN exhibited inherent cytotoxicity but mitigated HG-induced cytotoxicity in HCE-T cells.
  • GlcN reduced HG-induced reactive oxygen species (ROS) and cellular senescence.
  • GlcN modulated the expression of key proteins including KLF4, SIRT1, and the tight junction protein claudin-1.
  • SIRT1 inhibitors partially reversed the effects of GlcN on claudin-1 expression and ROS generation.

Conclusions:

  • Glucosamine demonstrates a protective effect against hyperglycemia-induced cellular damage in the corneal epithelium.
  • GlcN may rejuvenate the corneal epithelium by reducing oxidative stress and senescence, potentially through SIRT1-dependent pathways.
  • These findings suggest GlcN as a potential therapeutic agent for managing corneal complications associated with poor glycemic control.
Keywords:
Cell senescenceCorneal epithelial cellGlucosamineOxidative stressSIRT1

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