Icariin Ameliorates Streptozotocin-Induced Diabetic Retinopathy in Vitro and in Vivo

Hua Xin,Zhe-Zhu Gao,Guang-Yi Bai,Jing Liu,Hong Lu,Zhong-Cheng Xin,Feng Zhou,Guang-Yong Li,Tao Liu

doi:10.3390/ijms13010866

Abstract

This study investigated the effect of Icariin (ICA) supplementation on diabetic retinopathy (DR) in a streptozotocin-induced diabetic rat model system. Fifty Sprague Dawley rats were randomly distributed into a control group and a streptozotocin-induced diabetes group. Diabetic rats were randomly divided into two groups; one group received ICA 5 mg/kg/day for 12 weeks by oral gavage; the other group received saline gavage as a placebo. Retinal morphological changes, endothelial markers (RECA), collagen IV (Col-IV), vascular endothelial growth factor (VEGF), and neuropathic changes (Thy-1 and Brn3a expression) of the retinal ganglion cells (RGCs) were investigated. The effects of ICA at various concentrations (0, 101, 102, 103 nmol/mL) on neurite growth were investigated also in retinal ganglion cells (RGC) cultured from both diabetic and normal animals. Numerous pathological changes (deceased expression of RECA, VEGF, Thy-1, and Brn3a as well as decreased Collagen IV and Müller cell content) were noted in the retinal vessels of diabetic rats; these changes were attenuated in diabetic animals that received ICA. ICA enhanced neurite growth in RGC from both normal rats and diabetic rats in a dose dependent fashion. ICA may be useful in the treatment of diabetic retinopathy. Further investigations are indicated.

Highlights

Diabetic retinopathy (DR) is a leading cause of post-natal blindness and one of the most common complications of diabetes [1,2]
We investigated the effects of ICA on regulation RECA and collagen IV (Col-IV) expression in retinal endothelium and Thy-1 and Brn3a expression in retinal ganglion cells (RGCs) from rats with Streptozotocin-Induced
At the end of study mean body weight was decreased significantly, and final fasting serum glucose level increased in diabetic rats compared to sham controls (Table 1, P for difference < 0.01)

Summary

Introduction

Diabetic retinopathy (DR) is a leading cause of post-natal blindness and one of the most common complications of diabetes [1,2]. Prevalence of retinopathy within 20 years of diagnosis [3]. Microvascular lesions such as microaneurysms, increased vascular permeability caused by the breakdown of the blood-retinal barrier (BRB), and capillary dropout are thought to be key causes of DR [4,5,6]. The sole purpose of retinal circulation is to support the metabolic demands of the inner retinal neurons and glial; these cells may be damaged by the diabetic state. Are the sole output neurons from the eyes, assuming the critical role of transmitting visual signals to the higher visual center at the brain cortex before signal processing.

Methods

Results

Conclusion