Abstract
Retinal apoptosis plays a critical role in the progression of diabetic retinopathy (DR), a common diabetic complication. Currently, the tight control of blood glucose levels is the standard approach to prevent or delay the progression of DR. However, prevalence of DR among diabetic patients remains high. Focusing on natural nutrients or herbal medicines that can prevent or delay the onset of diabetic complications, we administered an ethanol extract of the aerial portion of Osteomeles schwerinae (OSSCE), a Chinese herbal medicine, over a period of 17 weeks to spontaneously diabetic Torii (SDT) rats. OSSCE was found to ameliorate retinal apoptosis through the regulation of advanced glycation end product (AGE) accumulation, oxidative stress, and mitochondrial function via the inhibition of NF-κB activity, in turn, through the downregulation of PKCδ, P47phox, and ERK1/2. We further demonstrated in 25 mM glucose-treated human retinal microvascular endothelial cells (HRMECs) that hyperoside (3-O-galactoside-quercetin), quercitrin (3-O-rhamnoside-quercetin), and 2″-O-acetylvitexin (8-C-(2″-O-acetyl-glucoside)-apigenin) were the active components of OSSCE that mediated its pharmacological action. Our results provide evidence that OSSCE is a powerful agent that may directly mediate a delay in the development or disease improvement in patients of DR.
Highlights
Diabetic retinopathy (DR) is common long-term microvascular complication of diabetes and is a microcirculation disorder that accounts for the large majority of cases of visual impairmentNutrients 2019, 11, 546; doi:10.3390/nu11030546 www.mdpi.com/journal/nutrientsNutrients 2019, 11, 546 in working-age adults [1]
We have previously reported that Osteomeles schwerinae (OSSCE) reduces the advanced glycation end product (AGE)/RAGE binding interaction and the expression of TGF-β1 by pERK1/2, p38MAPK, and IκB phosphorylation in mouse glomerular mesangial cells under diabetic conditions [20]
We investigated the inhibitory effects of OSSCE on AGE accumulation and retinal cell apoptosis in spontaneously diabetic Torii (SDT) rats
Summary
Diabetic retinopathy (DR) is common long-term microvascular complication of diabetes and is a microcirculation disorder that accounts for the large majority of cases of visual impairmentNutrients 2019, 11, 546; doi:10.3390/nu11030546 www.mdpi.com/journal/nutrientsNutrients 2019, 11, 546 in working-age adults [1]. Changes in DR include the apoptosis of peripheral blood cells, microvascular occlusion, vascular leakage, and microaneurysm [2]. Form the first barrier that senses changes in the blood glucose. Two hallmarks of human retinal cell loss in chronic diabetes have been reported—the loss of the blood–retinal barrier integrity and direct effects on metabolism in the neural retina [3]. The diabetic metabolic influence on retinal neurons leads to an increase in apoptosis, which, in turn, causes the breakdown of the blood–retinal barrier. The retinal neuron cells begin to die soon after the onset of streptozotocin (STZ)-induced diabetes in an experimental rat model. The increase in frequency of apoptosis occurred after only one month of induction, and a similar increase was noted in human retinas after six years of diabetes [4]. The prevalence of DR remains high [5]
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