Suresh Kumar Gupta1, Hanuman Prasad Sharma2, Ujjalkumar Das3, Thirumurthy Velpandian3, Ravi Saklani2. 1. Department of Pharmacology, Delhi Institute of Pharmaceutical Sciences and Research (DIPSAR), M.B. Road, Pushp Vihar Sector III, New Delhi, 110017, India. skgup@hotmail.com. 2. Department of Pharmacology, Delhi Institute of Pharmaceutical Sciences and Research (DIPSAR), M.B. Road, Pushp Vihar Sector III, New Delhi, 110017, India. 3. Ocular Pharmacology and Pharmacy Division, Dr. R. P. Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110 029, India.
Abstract
PURPOSE: The current study was conducted to explore the potential of rutin in preventing sight-threatening diabetic retinopathy. METHODS: Wistar albino rats (either sex) weighing 200-225 g were intraperitoneally injected with 45 mg/kg streptozotocin (pH 4.5). Rats having blood glucose ≥ 300 mg/dL were divided into two groups (n = 8; each group). Group I served as diabetic control and received normal saline p.o. Group II received rutin 50 mg/kg p.o. for 24 weeks. At the end of 24 weeks, retinal fundus and fluorescein imaging were done, rats were killed, and retinal biochemical assessments were conducted. Moreover, ocular pharmacokinetics of rutin was assessed in the normal rats after a single oral dose of 50 mg/kg. RESULTS: Rutin treatment significantly (p < 0.001) lowered retinal vascular endothelial growth factor, tumor necrosis factor-α, and aldose reductase. Rutin treatment significantly (p < 0.001) elevated the levels of total antioxidant capacity of the retinas. Fundus examination of rutin-treated group showed significantly lower tortuosity index and normal fluorescein angiography. Rutin was detected in the retina as well as in aqueous humor of normal rats. CONCLUSION: Rutin treatment significantly arrested the biochemical disturbances of diabetic retinopathy. The distribution of orally ingested rutin in ocular tissues further substantiate its site-specific action.
PURPOSE: The current study was conducted to explore the potential of rutin in preventing sight-threatening diabetic retinopathy. METHODS: Wistar albino rats (either sex) weighing 200-225 g were intraperitoneally injected with 45 mg/kg streptozotocin (pH 4.5). Rats having blood glucose ≥ 300 mg/dL were divided into two groups (n = 8; each group). Group I served as diabetic control and received normal saline p.o. Group II received rutin 50 mg/kg p.o. for 24 weeks. At the end of 24 weeks, retinal fundus and fluorescein imaging were done, rats were killed, and retinal biochemical assessments were conducted. Moreover, ocular pharmacokinetics of rutin was assessed in the normal rats after a single oral dose of 50 mg/kg. RESULTS:Rutin treatment significantly (p < 0.001) lowered retinal vascular endothelial growth factor, tumor necrosis factor-α, and aldose reductase. Rutin treatment significantly (p < 0.001) elevated the levels of total antioxidant capacity of the retinas. Fundus examination of rutin-treated group showed significantly lower tortuosity index and normal fluorescein angiography. Rutin was detected in the retina as well as in aqueous humor of normal rats. CONCLUSION:Rutin treatment significantly arrested the biochemical disturbances of diabetic retinopathy. The distribution of orally ingested rutin in ocular tissues further substantiate its site-specific action.
Authors: Kegao Liu; James D Akula; Christopher Falk; Ronald M Hansen; Anne B Fulton Journal: Invest Ophthalmol Vis Sci Date: 2006-06 Impact factor: 4.799