Hesperidin Prevents Retinal and Plasma Abnormalities in Streptozotocin-Induced Diabetic Rats

Molecules

Xiupu Shi²  Sha Liao¹  Huijuan Mi²  Changrun Guo²  Dongli Qi²  Fei Li²  Chunfeng Zhang² 

[1] College of Life Sciences, Northwest University, Taibai Road 229, Xi’an 710069, China;State Key Laboratory of Natural Products and Functions, China Pharmaceutical University, No. 24 Tongjiaxiang, Nanjing 210009, China;

关键词: hesperidin;    diabetic retinopathy;    anti-angiogenic effect;    aldose reductase activity;    AGEs accumulation;   

DOI  :  10.3390/molecules171112868

来源: mdpi

【 摘 要 】

Diabetic retinopathy is a complex disease that potentially involves increased production of advanced glycosylation end products (AGEs) and elevated aldose reductase (AR) activity, which are related with oxidative stress and inflammation. The aim of this study was to investigate the effects of hesperidin on retinal and plasma abnormalities in streptozotocin-induced diabetic rats. Hesperidin (100, 200 mg/kg daily) was given to diabetic rats for 12 weeks. The blood-retina breakdown (BRB) was determined after 2 weeks of treatment followed by the measurement of related physiological parameters with ELISA kits and immunohistochemistry staining at the end of the study. Elevated AR activity and blood glucose, increased retinal levels of vascular endothelial growth factor (VEGF), ICAM-1, TNF-α, IL-1β and AGEs as well as reduced retina thickness were observed in diabetic rats. Hesperidin treatment significantly suppressed BRB breakdown and increased retina thickness, reduced blood glucose, AR activity and retinal TNF-α, ICAM-1, VEGF, IL-1β and AGEs levels. Furthermore, treatment with hesperidin significantly reduced plasma malondialdehyde (MDA) levels and increased SOD activity in diabetic rats. These data demonstrated that hesperidin attenuates retina and plasma abnormalities via anti-angiogenic, anti-inflammatory and antioxidative effects, as well as the inhibitory effect on polyol pathway and AGEs accumulation.

【 授权许可】

CC BY   
© 2012 by the authors; licensee MDPI, Basel, Switzerland.