Curcumin suppresses oxidative stress via regulation of ROS/NF-κB signaling pathway to protect retinal vascular endothelial cell in diabetic retinopathy

Jiang Huang,Yuhong You,Quanyong Yi,Xiaoyan Ji,Weijie Zou,Yao Chen,Guoxu Xu,Weifeng Luo,Fangfang Ji,Ji Zhang,Yi Li,Tongtong Niu

doi:10.1007/s13273-021-00144-7

Abstract

BackgroundThe retinal vascular endothelial cells can be damaged by oxidative stress even in the early stage of diabetic retinopathy (DR). This study aimed to investigate the protective effect of curcumin on the rat retinal vascular endothelial cells (RRVECs) in high glucose circumstance.ObjectiveThe cultured RRVECs were identified and characterized by both of vWF and CD31 immunofluorescence expression. The activation of ROS/NF-κB signal pathway was examined by electrophoretic Mobility Shift Assay (EMSA), immunohistochemistry and Western blot; the apoptosis of RRVECs was tested by flow cytometry.ResultsWe found that curcumin reduced the reactive oxygen species (ROS) and relieved the apoptosis in RRVECs exposed to the high glucose by flow cytometry. It was revealed that the increased activity of NF-κB and phosphorylated NF-κB in RRVECs induced by high glucose concentration was significantly suppressed by curcumin.ConclusionWe concluded that curcumin could suppress the oxidative stress via regulation of NF-κB signal to protect the RRVECs in DR.

Highlights

Diabetic retinopathy (DR) is one of the most serious complications of diabetes mellitus and a leading blindness disease in the world
The ultrastructure changes in rat retinal vascular endothelial cells (RRVECs) were examined by transmission electron microscopy to detect whether curcumin could reduce the damage caused by high glucose concentration
In the high glucose group, the activity of NF-κB/DNA binding was increased, whereas, after curcumin treatment, the NF-κB activity was significantly declined. These results demonstrated that oxidative stress induced by high glucose could activate NF-κB as well as the phosphorylated NF-κB, and curcumin could suppress the activity of NF-κB by anti-oxidative stress to protect the RRVECs exposed to high glucose

Summary

Introduction

Diabetic retinopathy (DR) is one of the most serious complications of diabetes mellitus and a leading blindness disease in the world. The retinal vascular endothelial cells can be damaged by oxidative stress even in the early stage of diabetic retinopathy. Typical early changes in the retinal vasculature of diabetic eyes are pericyte loss, basement membrane thickening, the retinal vascular endothelial cell (RVEC) proliferation and blood-retina barrier leakage[5 6]. Oxidative stress activates multiple pathways in the cell, including signaling cascades, cell apoptosis, and transcription factors, which in turn cause the pathophysiological changes of the retinal vasculature in diabetic retinopathy. The RVECs are key participants in diabetic retinopathy They supply oxygen and nutrients for the normal metabolism of the retina, and contribute to the blood-retinal barrier that protects the retina [11 12]. Some studies [13–15] have shown that NF-κB regulates the expression of angiogenic factors in vascular endothelial cells and induces neovascularization in diabetic retinopathy

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