OSSC1E-K19, a novel phytochemical component of Osteomeles schwerinae, prevents glycated albumin-induced retinal vascular injury in rats

Abstract

In the pathophysiology of diabetic retinopathy (DR), advanced glycation end products (AGEs) and vascular endothelial growth factor (VEGF) are thought to have important roles. It is known that VEGF causes a breakdown of the blood-retinal barrier (BRB) and retinal neovascularization; however, how AGEs affect the retina has largely remained elusive. OSSC1E-K19 is a novel phytochemical component of Osteomeles schwerinae. The objective of the present study was to evaluate the protective effects of OSSC1E-K19 on retinal vascular injury in AGE-modified rat serum albumin (AGE-RSA)-induced retinopathy. AGE-RSA-injected rat eyes were used investigate the protective effects of OSSC1E-K19 on BRB breakdown. Intravitreal injection of OSSC1E-K19 prevented AGE-RSA-induced BRB breakdown and decreased retinal VEGF expression in retinal vessels. In addition, OSSC1E-K19 inhibited the loss of occludin, a significant tight junction protein. These results supported the potential therapeutic utility of OSSC1E-K19 for retinal vascular permeability diseases.

Improvement in Diabetic Retinopathy through Protection against Retinal Apoptosis in Spontaneously Diabetic Torii Rats Mediated by Ethanol Extract of Osteomeles schwerinae C.K. Schneid

“…Another novel compound from OSSCE, 4-hydroxy-3′,5′-dimethoxybiphenyl-(1,1′-biphenyl)-3-O-β-D-glucopyranoside (referred to as K19), inhibits the nonenzymatic formation of AGE and the cross-linking of AGE to collagen in vitro. An intravitreal injection of K19 into the AGE-modified rat serum albumin (AGE-RSA)-injected Sprague-Dawley (SD) rats inhibited a retinal vascular leakage by suppressing the expression of vascular endothelial growth factor (VEGF) and by preventing the loss of occludin, an important tight junction protein [19]. We have previously reported that OSSCE reduces the 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].…”