An Aqueous Extract of Radix Astragali,Angelica sinensis, andPanax notoginsengIs Effective in Preventing Diabetic Retinopathy

Dehong Gao,Xiumin Li,Ming Liu,Shuyu Yang,Xuejun Li,Mei Xue,Mingxing Yang,Zhipeng Li,Yijuan Guo,Suhuan Liu,Zhimin Ou

doi:10.1155/2013/578165

Abstract

Diabetic retinopathy (DR), in which inflammation has been implicated playing important roles, is one of the most common diabetes complications. Dang Gui Bu Xue Tang (DBT), an aqueous extract of Radix Astragali and Radix Angelica sinensis, is a classical prescription in Traditional Chinese Medicine for treating inflammation and ischemic diseases. Here, we investigated the effects of a modified recipe of DBT, with addition of Panax notoginseng, in treating diabetic retinopathy. An aqueous extract of Radix Astragali, Radix Angelica sinensis, and Panax notoginseng (RRP) was given to Goto-Kakizaki (GK) rats and streptozotocin-induced Sprague-Dawley (SD) rats. Leukostasis, vascular leakage, and acellular capillaries in retinal vasculature of animals were determined. Expression of retinal inflammatory biomarkers was assessed. We found that RRP reduced leukostasis, acellular capillaries, and vascular leakage compared to diabetic control rats. We also found that RRP decreased the expression of inflammatory factors including IL-1β, IL-6, TNF-α, NF-κB, MCP-1, ICAM-1, or VCAM-1 in the retinas of GK rats and reversed high glucose-induced inhibition of endothelial cell migration and proliferation in vitro. We conclude that RRP has a potent effect in preventing the pathogenesis and/or progression of DR and thus may serve as a promising nontoxic therapeutic approach of DR.

Highlights

Diabetic retinopathy (DR) is a major cause of blindness among working-age adults in developed countries
We showed here that RRP treatment prevented leukocyte adherent to the vascular wall, attenuated vascular leakage, inhibited formation of acellular capillaries, the three early signature pathologies of diabetic retinopathy, ameliorated the retina damage and prevented DR
Proinflammatory cytokines and chemokines activate endothelium to increase expression of adhesion molecules and chemokines, by which leukocytes/monocytes were mediated to attach to the vessel wall and transmigrate through the endothelium [1]

Summary

Introduction

Diabetic retinopathy (DR) is a major cause of blindness among working-age adults in developed countries. Hyperglycemia induces increased oxidative stress [2], inflammation [3], and vascular dysfunction through multiple cellular pathways and results in increased leukostasis [4, 5], vascular permeability [6], and formation of acellular capillaries [7]. Leukostasis has been found significantly increased in retinas of diabetic animals and might contribute to retinal vascular permeability and capillary nonperfusion in DR [8]. Previous studies have reported that increased endothelial/pericyte ratio [12], subretinal accumulation of activated microglia/macrophages [13], increased vascular endothelial growth factor (VEGF) production in certain ocular tissue [14], and increased number of acellular capillaries [15], known as early histological changes of diabetic retinopathy, were confirmed in GK rats

Methods

Results

Conclusion