4.7 Article

Treatment with hydrogen sulfide alleviates streptozotocin-induced diabetic retinopathy in rats

Journal

BRITISH JOURNAL OF PHARMACOLOGY
Volume 169, Issue 3, Pages 619-631

Publisher

WILEY
DOI: 10.1111/bph.12163

Keywords

hydrogen sulfide; streptozotocin; diabetic retinopathy; oxidative stress; inflammation

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Background and Purpose Retinopathy, as a common complication of diabetes, is a leading cause of reduced visual acuity and acquired blindness in the adult population. The aim of present study was to investigate the therapeutic effect of hydrogen sulfide on streptozotocin (STZ)-induced diabetic retinopathy in rats. Experimental Approach Rats were injected with a single i.p. injection of STZ (60mg center dot kg(-1)) to induce diabetic retinopathy. Two weeks later, the rats were treated with NaHS (i.p. injection of 0.1mL center dot kg(-1)center dot d(-1) of 0.28mol center dot L-1 NaHS, a donor of H2S) for 14 weeks. Key Results Treatment with H2S had no significant effect on blood glucose in STZ-induced diabetic rats. Treatment with exogenous H2S enhanced H2S levels in both plasma and retinas of STZ-induced diabetic rats. Treatment with H2S in STZ-treated rats improved the retinal neuronal dysfunction marked by enhanced amplitudes of b-waves and oscillatory potentials and expression of synaptophysin and brain-derived neurotrophic factor, alleviated retinal vascular abnormalities marked by reduced retinal vascular permeability and acellular capillary formation, decreased vitreous VEGF content, down-regulated expressions of HIF-1 alpha and VEGFR2, and enhanced occludin expression, and attenuated retinal thickening and suppressed expression of extracellular matrix molecules including laminin 1 and collagen IV3 expression in retinas of STZ-induced diabetic rats. Treatment with H2S in retinas of STZ-induced diabetic rats abated oxidative stress, alleviated mitochondrial dysfunction, suppressed NF-B activation and attenuated inflammation. Conclusions and Implications Treatment with H2S alleviates STZ-induced diabetic retinopathy in rats possibly through abating oxidative stress and suppressing inflammation.

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