Abstract
BackgroundOxidative stress and inflammation are implicated in the pathogenesis of retinopathy in diabetes. The aim of this study is to examine the effect of curcumin, a polyphenol with antioxidant and anti-inflammatory properties, on diabetes-induced oxidative stress and inflammation in the retina of rats.MethodsA group of streptozotocin-induced diabetic rats received powdered diet supplemented with 0.05% curcumin (w/w), and another group received diet without curcumin. The diets were initiated soon after induction of diabetes, and the rats were sacrificed 6 weeks after induction of diabetes. The retina was used to quantify oxidative stress and pro-inflammatory markers.ResultsAntioxidant capacity and the levels of intracellular antioxidant, GSH (reduced form of glutathione) levels were decreased by about 30–35%, and oxidatively modified DNA (8-OHdG) and nitrotyrosine were increased by 60–70% in the retina of diabetic rats. The levels of interleukin-1β (IL-1β) and vascular endothelial growth factor (VEGF) were elevated by 30% and 110% respectively, and the nuclear transcription factor (NF-kB) was activated by 2 fold. Curcumin administration prevented diabetes-induced decrease in the antioxidant capacity, and increase in 8-OHdG and nitrotyrosine; however, it had only partial beneficial effect on retinal GSH. Curcumin also inhibited diabetes-induced elevation in the levels of IL-1β, VEGF and NF-kB. The effects of curcumin were achieved without amelioration of the severity of hyperglycemia.ConclusionThus, the beneficial effects of curcumin on the metabolic abnormalities postulated to be important in the development of diabetic retinopathy suggest that curcumin could have potential benefits in inhibiting the development of retinopathy in diabetic patients.
Highlights
Oxidative stress and inflammation are implicated in the pathogenesis of retinopathy in diabetes
We have shown that intravitreal injection of interleukin-1β (IL-1β) to the normal rats increases retinal capillary cell apoptosis and histopathology; and these IL1β-induced changes in the retinal capillaries of normal rats are similar to those observed in diabetes [13]
Administration of curcumin prevented diabetes-induced decrease in the total antioxidant capacity of the retina; the values obtained from normal control rats and in curcumin-treated diabetic rats were similar (Figure 2a)
Summary
Oxidative stress and inflammation are implicated in the pathogenesis of retinopathy in diabetes. Abnormalities in retinal metabolism, including elevated polyol pathway activity, increased nonenzymatic glycation and advanced glycation end products, oxidative stress, protein kinase C (PKC) activity [1,2,3,4,5], contribute to the development of retinopathy, but the exact mechanism is still elusive. Recent studies have compared the development of diabetic retinopathy to the low-level chronic inflammatory disease; the retinal capillaries become nonperfused and ischemic, and the number of platelet-fibrin thrombi increases in diabetes [10]. IL-1β is shown to increase the expression of vascular endothelial growth factor (VEGF) in retinal endothelial cells [14], and VEGF is implicated in the development of diabetic retinopathy [15]
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