Dietary taurine supplementation ameliorates diabetic retinopathy via anti-excitotoxicity of glutamate in streptozotocin-induced Sprague-Dawley rats.
The purpose of this study was to investigate whether taurine ameliorate the diabetic retinopathy, and to further explore the underlying mechanisms. The Sprague-Dawley rats were injected with streptozotocin to establish experimental diabetic model, then fed without or with 1.2% taurine for additional 4-12 weeks. After that, the protective effects of dietary taurine supplementation on diabetic retinopathy were estimated. Our results showed that chronic taurine supplement effectively improved diabetic retinopathy as changes of histopathology and ultrastructure. The supplementation could not lower plasma glucose concentration (P > 0.05), but caused an elevation in taurine content and a decline in levels of glutamate and gamma-aminobutyric acid (GABA) in diabetic retina (P < 0.05). Moreover, chronic taurine supplementation increased glutamate transporter (GLAST) expression (P < 0.05), decreased intermediate filament glial fibrillary acidic protein (GFAP) and N-methyl-D: -aspartate receptor subunit 1 (NR1) expression in diabetic retina (P < 0.05). These results demonstrated that chronic taurine supplementation ameliorates diabetic retinopathy via anti-excitotoxicity of glutamate in rats.
Yu
Xiaoping
X
Department of Public Health, School of Preclinical Medicine, Chengdu Medical College, 601 Rongdu Road, Jinniu District, Chengdu 610081, China.
Xu
Zhaoxia
Z
Mi
Mantian
M
Xu
Hongxia
H
Zhu
Jundong
J
Wei
Na
N
Chen
Ka
K
Zhang
Qianyong
Q
Zeng
Kaihong
K
Wang
Jian
J
Chen
Fang
F
Tang
Yong
Y
D027322:Amino Acid Transport System X-AG / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015153:Blotting, Western; D001835:Body Weight / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000473:pathology; D003930:Diabetic Retinopathy / Q000188:drug therapy* / Q000473:pathology; D019587:Dietary Supplements; D018691:Excitatory Amino Acid Antagonists; D027341:Excitatory Amino Acid Transporter 1 / Q000096:biosynthesis; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000096:biosynthesis; D012160:Retina / Q000473:pathology / Q000648:ultrastructure; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013654:Taurine / Q000378:metabolism / Q000627:therapeutic use*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D027322:Amino Acid Transport System X-AG; D001786:Blood Glucose; D018691:Excitatory Amino Acid Antagonists; D027341:Excitatory Amino Acid Transporter 1; D005904:Glial Fibrillary Acidic Protein; C409466:NR1 NMDA receptor; D016194:Receptors, N-Methyl-D-Aspartate; C493392:Slc1a3 protein, rat; D013654:Taurine; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid