Table of Contents Author Guidelines Submit a Manuscript
Journal of Diabetes Research
Volume 2018 (2018), Article ID 8193523, 11 pages
Research Article

Vitamin D3 Protects against Diabetic Retinopathy by Inhibiting High-Glucose-Induced Activation of the ROS/TXNIP/NLRP3 Inflammasome Pathway

1Department of Ophthalmology, Anhui Provincial Hospital The First Affiliated Hospital of University of Science and Technology of China, Hefei 230001, China
2Department of Ophthalmology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China
3Department of Ophthalmology, Shanghai First People’s Hospital, Shanghai Jiao Tong University, Shanghai 200080, China
4Department of Ophthalmology, Shanghai TCM-Integrated Hospital, Shanghai University of TCM, 230 Baoding Road, Shanghai 200082, China

Correspondence should be addressed to Chunxia Li

Received 17 July 2017; Revised 15 October 2017; Accepted 16 November 2017; Published 22 February 2018

Academic Editor: Amany Tawfik

Copyright © 2018 Li Lu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Purpose. This study aimed to evaluate the mechanisms underlying the effects of 1,25-dihydroxyvitamin D (vitamin D3) on diabetes-induced retinal vascular damage and retinal vascular endothelial cell apoptosis. Methods. Diabetic and control rats were randomly assigned to receive vitamin D3 or vehicle for 6 months. Additionally, human retinal microvascular endothelial cells (HRMECs) were incubated in normal or high-glucose medium with or without vitamin D3. Morphological changes in retinal tissues and retinal vascular permeability were examined, and cellular apoptosis was detected by fluorescence staining. Intracellular reactive oxygen species (ROS) levels were determined using fluorescent probes. Proteins were examined by Western blotting. Results. Vitamin D3 significantly downregulated intracellular ROS and inhibited TRX-interacting protein (TXNIP)/NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome pathway activation. Additionally, vitamin D3 reduced vascular endothelial growth factor (VEGF) expression and the Bax/Bcl-2 ratio. These changes were associated with retinal recovery and with decreases in retinal vascular permeability and retinal capillary cell apoptosis. Conclusions. Vitamin D3 decreases diabetes-induced ROS and exerts protective effects against retinal vascular damage and cell apoptosis in association with inhibition of the ROS/TXNIP/NLRP3 inflammasome pathway. Understanding the mechanisms of action of vitamin D3 has important implications for preventing and treating inflammatory-related illnesses such as diabetic retinopathy.