Food-advanced glycation end products aggravate the diabetic vascular complications via modulating the AGEs/RAGE pathway.
10.1016/S1875-5364(16)30101-7
- Author:
Xing LV
1
;
Gao-Hong LV
1
;
Guo-Ying DAI
1
;
Hong-Mei SUN
2
;
Hui-Qin XU
3
Author Information
1. Department of Pharmacology, College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; Jiang Su key Laboratory for Efficacy and Safety Evaluation of Chinese Medicine, Nanjing 210023, China.
2. Department of Pharmacology, College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; Department of Chinese Medicine Resources, College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China.
3. Department of Pharmacology, College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; Jiang Su key Laboratory for Efficacy and Safety Evaluation of Chinese Medicine, Nanjing 210023, China. Electronic address: hqxu309@aliyun.com.
- Publication Type:Journal Article
- Keywords:
AGEs/RAGE/ROS pathway;
Advanced glycation end products;
Diabetic vascular complications;
Reactive oxygen species;
c-Reactive protein
- MeSH:
Animals;
Diabetes Mellitus, Experimental;
complications;
metabolism;
Diabetic Angiopathies;
genetics;
metabolism;
Diet;
adverse effects;
Glycation End Products, Advanced;
metabolism;
Humans;
Interleukin-6;
metabolism;
Kidney;
metabolism;
Male;
Mice;
Mice, Inbred C57BL;
Oxidative Stress;
Pancreas;
metabolism;
Reactive Oxygen Species;
metabolism;
Receptor for Advanced Glycation End Products;
genetics;
metabolism;
Superoxide Dismutase;
metabolism;
Tumor Necrosis Factor-alpha;
metabolism
- From:
Chinese Journal of Natural Medicines (English Ed.)
2016;14(11):844-855
- CountryChina
- Language:English
-
Abstract:
The aim of this study was to investigate the effects of high-advanced glycation end products (AGEs) diet on diabetic vascular complications. The Streptozocin (STZ)-induced diabetic mice were fed with high-AGEs diet. Diabetic characteristics, indicators of renal and cardiovascular functions, and pathohistology of pancreas, heart and renal were evaluated. AGEs/RAGE/ROS pathway parameters were determined. During the experiments, the diabetic mice exhibited typical characteristics including weight loss, polydipsia, polyphagia, polyuria, high-blood glucose, and low-serum insulin levels. However, high-AGEs diet effectively aggravated these diabetic characteristics. It also increased the 24-h urine protein levels, serum levels of urea nitrogen, creatinine, c-reactive protein (CRP), low density lipoprotein (LDL), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in the diabetic mice. High-AGEs diet deteriorated the histology of pancreas, heart, and kidneys, and caused structural alterations of endothelial cells, mesangial cells and podocytes in renal cortex. Eventually, high-AGEs diet contributed to the high-AGE levels in serum and kidneys, high-levels of reactive oxygen species (ROS) and low-levels of superoxide dismutase (SOD) in serum, heart, and kidneys. It also upregulated RAGE mRNA and protein expression in heart and kidneys. Our results showed that high-AGEs diet deteriorated vascular complications in the diabetic mice. The activation of AGEs/RAGE/ROS pathway may be involved in the pathogenesis of vascular complications in diabetes.
