April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Topical Administration of Kinin B1 Receptor Antagonist FV-60135-02 Inhibits Retinal Inflammation in Streptozotocin-Diabetic Rats
Author Affiliations & Notes
  • M. Pouliot
    School of Optometry,
    Department of Physiology,
    University of Montreal, Montreal, Quebec, Canada
  • S. Talbot
    Department of Physiology,
    University of Montreal, Montreal, Quebec, Canada
  • E. Vaucher
    School of Optometry,
    University of Montreal, Montreal, Quebec, Canada
  • D. Pruneau
    Fovea Pharmaceuticals, Paris, France
  • R. Couture
    Department of Physiology,
    University of Montreal, Montreal, Quebec, Canada
  • Footnotes
    Commercial Relationships  M. Pouliot, None; S. Talbot, None; E. Vaucher, None; D. Pruneau, None; R. Couture, None.
  • Footnotes
    Support  FRSQ Vision Research Network, CIHR, Foundation Fighting Blindness
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 5611. doi:
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      M. Pouliot, S. Talbot, E. Vaucher, D. Pruneau, R. Couture; Topical Administration of Kinin B1 Receptor Antagonist FV-60135-02 Inhibits Retinal Inflammation in Streptozotocin-Diabetic Rats. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5611.

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

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Abstract

Purpose: : Recent studies proposed that kinin B1 receptor (B1R) is involved in retinal vascular damage in diabetic rats, i.e. changes in vasoreactivity and breakdown of the blood-retinal barrier. B1R is upregulated in retina of Streptozotocin (STZ)-diabetic rats by oxidative stress, suggesting that treatment with B1R antagonists could improve retina homeostatis in diabetes. The present study aims at determining whether topical administration of a B1R antagonist, FV-60135-02, could reverse retinal vascular hyperpermeability, leukostasis and inflammatory mediators putatively involved in diabetic retinopathy.

Methods: : Wistar rats were rendered diabetic by a single injection of STZ (65 mg/kg, i.p.). 7 days later, rats were treated twice a day with one eye drop application of FV-60135-02 (1% in saline) for a 7 day-period. On the last day of treatment, retinal vascular permeability, leukostasis and retinal mRNA levels of B1R, B2R, iNOS, eNOS, COX-2, ICAM-1, VEGFα, VEGF receptor type 2, IL-1β and HIF-1α were measured by quantitative RT-PCR.

Results: : Retinal plasma extravasation (Evans Blue/g wet tissue, n = 9-11) was significantly increased in STZ-diabetic rats (25.7 ± 1.9 µg) compared to control rats (19.6 ± 1.1 µg) and blocked by FV-60135-02 (19.9 ± 1.6 µg). Number of adherent leukocytes in retinal vessels was significantly increased in diabetic rats (164 ± 27, n = 5) compared to control rats (106 ± 38, n = 7) and decreased in diabetic rats treated with FV-60135-02 (111 ± 43, n = 7). mRNA levels of B1R, iNOS, COX-2, VEGF receptor type 2, IL-1β and HIF-1α were significantly increased in diabetic retinas compared to control rats and were back to control values by FV-60135-02.

Conclusions: : Topical application of kinin B1R antagonist is found as an effective and non-toxic approach to reverse increased vascular permeability and leukostasis in diabetes. B1R seems to have a pathological role in the early stage of diabetes by interacting with other factors involved in inflammation and retinal vascular damage.

Keywords: diabetic retinopathy • inflammation 
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