TITLE

1,25(OH)D-Mediated Amelioration of Aortic Injury in Streptozotocin-Induced Diabetic Rats

AUTHOR(S)
Li, Fengao; Liu, Ping; Zhang, Xin; Zhang, Qiuzi; Tang, Shaofang; Zhu, Mei; Qiu, Mingcai
PUB. DATE
December 2013
SOURCE
Inflammation;Dec2013, Vol. 36 Issue 6, p1334
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
In this study, a single tail vein injection of streptozotocin (STZ)-induced rat model was employed to study the effects of 1,25(OH)D supplementation, the active form of vitamin D, on diabetes-induced aortic injury. Aortas from different groups were assessed for histopathology, toll-like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88), and nuclear factor-kappa B (NF-κB) p65 expression by hematoxylin and eosin staining, immunohistochemistry staining, reverse transcription polymerase chain reaction, and Western blot analysis. High-dose 1,25(OH)D (0.3 μg/kg/day) significantly prevented diabetes-induced aortic pathological changes and collagen deposition and decreased the expression of TLR4, MyD88, and NF-κB at both mRNA and protein levels in the aorta of STZ-induced diabetic rats ( P < 0.01). In vitro studies in A7r5 cells (a rat embryonic thoracic aortic smooth muscle cell line) showed that high-dose glucose (25 mmol/L) enhanced TLR4 expression at both mRNA and protein levels by fourfold and twofold, respectively, at 24 h, which were significantly diminished by 1,25(OH)D (1 × 10 mol/L) by 50 and 36 %, respectively. Similar effects of high-dose 1,25(OH)D on the expression of MyD88 were observed. Our results indicate that vitamin D has protective effects on diabetes-induced aortic injury and attenuates the expressions of TLR4, MyD88, and NF-κB in diabetic rats.
ACCESSION #
91842248

 

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