June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Montelukast modulates diabetes-induced inflammation and electrophysiological changes in early diabetic retinopathy in the mouse
Author Affiliations & Notes
  • Reena Bapputty
    Pediatric Endocrinology, Case Western Reserve University, Cleveland, Ohio, United States
  • Ivy S Samuels
    Research Service, Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio, United States
  • Ramaprasad Talahalli
    Pediatric Endocrinology, Case Western Reserve University, Cleveland, Ohio, United States
  • Rose Anne Gubitosi-Klug
    Pediatric Endocrinology, Case Western Reserve University, Cleveland, Ohio, United States
  • Footnotes
    Commercial Relationships   Reena Bapputty, None; Ivy Samuels, None; Ramaprasad Talahalli, None; Rose Gubitosi-Klug, None
  • Footnotes
    Support  NEI R01-EY021535 and VA Merit Award I01BX002754
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 5219. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Reena Bapputty, Ivy S Samuels, Ramaprasad Talahalli, Rose Anne Gubitosi-Klug; Montelukast modulates diabetes-induced inflammation and electrophysiological changes in early diabetic retinopathy in the mouse. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5219.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose : Pro-inflammatory leukotrienes and cytokines have been implicated as mediators of inflammation in early diabetic retinopathy. In the current study we investigated the effect of montelukast, a leukotriene receptor antagonist, on 1) gene expression of inflammatory cascades in the retina and 2) diabetes-induced defects in the electroretinogram.

Methods : Montelukast (5mg/kg body weight) was given to mice immediately following the induction of diabetes. Gene expression of inflammatory leukotrienes and cytokines in the retina were quantified by real-time PCR. Electrical response of the RPE (dc-ERG) and the neural retina (a-wave and b-wave) was measured by ERG prior to sacrifice at 12-weeks of diabetes duration.

Results : Diabetes induced expression of leukotriene B4 receptors BLT1 (p=0.001) and BLT2 (p=0.001), in the retina, compared to non-diabetic control mice (ND). Montelukast treatment significantly inhibited gene expression of BLT1 (p=0.001) and BLT2 (p=0.001) in treated mice, compared to diabetic mice, and the values were comparable to non-diabetic mice. Montelukast treatment also significantly inhibited diabetes-induced expression of cytokine receptor, TNFR1, and intercellular adhesion molecule, ICAM1 in the retina in treated mice. Evaluation of the electroretinogram showed that diabetes caused significant damage to the physiology of the retina compared to ND mice and montelukast treatment improved the light-evoked responses of the inner retina (b-wave) and in the RPE (dc-ERG c-wave).

Conclusions : Leukotriene receptors BLT1 and BLT2 and TNFR1 contribute to diabetes-induced early inflammatory process in the retina. Montelukast protects the retina from diabetes-induced inflammation and improves the retinal function on ERG.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×