Ketorolac and (-)-Epicatechin change retinal GFAP and NRF2 expression on hyperglycemic CD1 mice

Area of Science:

• Biomedical Science
• Neuroscience
• Ophthalmology

Background:

• Hyperglycemia can induce preclinical retinal damage.
• Glial fibrillary acidic protein (GFAP) and nuclear factor erythroid 2-related factor 2 (Nrf2) are key markers in cellular stress and inflammation.
• Understanding modulators of these pathways is crucial for developing therapeutic strategies.

Purpose of the Study:

• To investigate the effects of (-)-Epicatechin and topical Ketorolac on GFAP and Nrf2 expression in a mouse model of induced hyperglycemia.
• To determine if these agents, administered alone or concurrently, offer protection against hyperglycemia-induced retinal damage.

Main Methods:

• A mouse model with induced hyperglycemia was utilized.
• Mice were treated with (-)-Epicatechin and/or topical Ketorolac for 8 weeks.
• Relative expression of GFAP and modulation of Nrf2 were assessed.

Main Results:

• Both GFAP and Nrf2 expression decreased in treatment groups over 8 weeks.
• While Nrf2 modulation was less pronounced, it correlated with decreased GFAP levels.
• The combined or individual treatments showed a trend towards reduced preclinical retinal damage.

Conclusions:

• (-)-Epicatechin and Ketorolac demonstrate a protective effect in the context of hyperglycemia.
• These agents appear to mitigate hyperglycemia-induced retinal inflammation and damage.
• Further research into these compounds could lead to novel therapeutic interventions for diabetic retinopathy.