Reverse Translational Study of Fenofibrate's Observed Effects in Diabetes-Associated Retinopathy
1Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences College of Pharmacy, Little Rock, Arkansas, USA.
Clinical and Translational Science
|December 21, 2016
Summary
Fenofibrate can reduce inflammatory chemokines and genes linked to abnormal blood vessel growth in retinal cells. This suggests a potential therapeutic role for fenofibrate in managing diabetic retinopathy.
Area of Science:
- Ophthalmology
- Endocrinology
- Molecular Biology
Background:
- Diabetic retinopathy is a leading cause of vision loss.
- Retinopathies involve increased inflammatory chemokines and aberrant retinal angiogenesis.
- Fenofibrate shows promise in reducing diabetic retinopathy progression.
Purpose of the Study:
- Investigate fenofibrate's effects on inflammatory chemokines.
- Examine fenofibrate's impact on genes associated with angiogenesis in retinal cells.
Main Methods:
- Retinal pigment epithelial cells (RPECs) were treated with IL-1β and varying concentrations of fenofibrate.
- Chemokine production (ENA-78, IL-8, RANTES) was measured using ELISA.
- Gene expression of ENA-78, ABCA1, and ABCG1 was analyzed via RT-PCR.
Main Results:
- IL-1β significantly increased ENA-78, IL-8, and RANTES production.
- Fenofibrate (25–50 μM) significantly reduced IL-1β-induced ENA-78 production.
- Fenofibrate decreased ENA-78 gene expression and expression of angiogenesis-related genes ABCA1 and ABCG1.
Conclusions:
- Fenofibrate mitigates the production of specific inflammatory chemokines in RPECs.
- Fenofibrate downregulates genes involved in angiogenesis, potentially impacting retinal vascularization.
- These findings support fenofibrate's potential therapeutic benefit in diabetic retinopathy by targeting inflammation and angiogenesis.
