Abstract
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.
Highlights
As a leading cause of blindness in middle age and older people, diabetic retinopathy (DR) is one of the most common complications of type 1 and type 2 diabetes [1,2]
Blood glucose levels were significantly increased in STZ-induced diabetic rats (p < 0.01), and treatment with Hsp and calcium dobesilate (CaD) led to a significant fall in blood glucose levels (p < 0.05)
Diabetic retinopathy is a complication induced by high blood glucose levels, and it has been confirmed by previous researches that the retinal and plasma abnormalities in diabetic rats are similar to that observed in diabetic patients [21,22]
Summary
As a leading cause of blindness in middle age and older people, diabetic retinopathy (DR) is one of the most common complications of type 1 and type 2 diabetes [1,2]. The exact mechanism by which hyperglycemia causes vascular disruption in retinopathy is not clear, it has been reported that, in addition to triggering oxidative stress along with inflammatory components [6], hyperglycemia is involved in the development of diabetic retinopathy by increasing the activity of aldose reductase (AR) [7] and protein kinase C (PKC) [8], as well as promoting nonenzymatic glycation and glycooxidation of proteins (AGEs) [9]. Free radicals as reactive oxygen species (ROS) are a strong stimulus for the release of proinflammatory cytokines, such as tumor necrosis factor-α(TNF-α) and interleukin 1β (IL-1β), which damage endothelial cells and play an important role in the pathogenesis of DR [10], and it has been reported that anti-inflammatory drugs could prevent early diabetic retinopathy via suppression of proinflammatory cytokines like TNF-α [11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
