Abstract
PurposeWe investigated the effect of long-term administration of supplement with trapa bispinosa roxb. extract (TBE) and lutein on the susceptibility of retinal blood flow regulation in type 2 diabetic mice.MethodsSix-week-old db/db mice were randomly divided into the untreated group (n = 6) and the treated group received the supplement with TBE and lutein (n = 6). The longitudinal changes in retinal blood flow responses to systemic hyperoxia and a flicker stimulation were evaluated every 2 weeks in diabetes db/db mice from age 8 to 14 weeks. The retinal blood flow was assessed using laser speckle flowgraphy. We also evaluated the expressions of glial fibrillary acid protein (GFAP) and vascular endothelial growth factor (VEGF) by immunofluorescence.ResultsThe resting retinal blood flow was steady and comparable between two groups throughout the study. In db/db mice with supplement, both blood flow responses were restored from 8 to 14 weeks of age compared with diabetic mice treated with the placebo. Supplement prevented the activation of GFAP and decreased the expression of VEGF detected by immunofluorescence compared with the diabetic mice treated with placebo.ConclusionWe found that the long-term administration of supplement with TBE and lutein improved the impaired regulation of retinal blood flow in response to systemic hyperoxia and flicker stimulation, suggesting that these supplements can prevent diabetic retinopathy by improving abnormal neurovascular coupling in type 2 diabetic mice.
Highlights
Diabetes is a chronic disease that is increasingly prevalent worldwide (Saeedi et al, 2019), and diabetic retinopathy continues as a leading cause of blindness (Bourne et al, 2013)
During the period of experiments, there were no significant differences between treated and untreated mice in terms of body weight, blood glucose level, diastolic BP (DBP), Intraocular pressure (IOP), and ocular perfusion pressure (OPP)
Because we have previously found that retinal glial cells play important roles in the change in retinal blood flow in response to systemic hyperoxia (Song et al, 2016) and flicker stimulation (Song et al, 2015), the impaired blood flow response to hyperoxia and flicker observed in diabetic mice may be caused by the Müller glial cell dysfunction induced by the accumulation of advanced glycation end (AGE)
Summary
Diabetes is a chronic disease that is increasingly prevalent worldwide (Saeedi et al, 2019), and diabetic retinopathy continues as a leading cause of blindness (Bourne et al, 2013). In terms of diabetic retinopathy, our recent study revealed that retinal blood flow does not respond to systemic hyperoxia and flicker stimulations in db/db mice with early type 2 diabetes and no apparent changes in resting retinal perfusion (Hanaguri et al, 2021), indicating that early detection of the impaired retinal flow regulation and prompt treatment may protect retinal tissue and prevent or slow the development of irreversible retinopathy Based on these previous findings, we test the hypothesis that the long-term administration of TBE and lutein supplements may have beneficial effects on the impaired retinal blood flow regulation to flicker stimulation/ systemic hyperoxia, and the retinal glial activation and the overexpression of vascular endothelial growth factor (VEGF) in the type 2 diabetic mouse retina
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