Literature DB >> 23488985

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

Yan-Fang Si1, Jun Wang, Juan Guan, Li Zhou, Yu Sheng, Juan Zhao.   

Abstract

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 (60 mg·kg⁻¹) to induce diabetic retinopathy. Two weeks later, the rats were treated with NaHS (i.p. injection of 0.1 mL·kg⁻¹·d⁻¹ of 0.28 mol·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-1α and VEGFR2, and enhanced occludin expression, and attenuated retinal thickening and suppressed expression of extracellular matrix molecules including laminin β1 and collagen IVα3 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-κB 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.
© 2013 The Authors. British Journal of Pharmacology © 2013 The British Pharmacological Society.

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Year:  2013        PMID: 23488985      PMCID: PMC3682709          DOI: 10.1111/bph.12163

Source DB:  PubMed          Journal:  Br J Pharmacol        ISSN: 0007-1188            Impact factor:   8.739


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