Abstract：
:Periodontitis is a complication of diabetes mellitus, and the two diseases are highly associated with the dysfunction of inflammatory mediators. 25-hydroxyvitamin D(3) (25(OH)D(3)) plays a pivotal role in inflammatory modulation, but little is known about its effects on the progression of diabetic periodontitis and the underlying mechanism. In this paper, we showed that 25(OH)D(3) ameliorated experimental periodontitis in diabetic mice. The intraperitoneal administration of 25(OH)D(3) to streptozotocin-induced diabetic mice reduced fasting glucose and serum TNF-α levels, leading to decreased alveolar bone loss. Western blot analyses of gingival epithelia showed that vitamin D receptor (VDR) and protein tyrosine phosphatase N2 (PTPN2) were upregulated, while the expression of NF-κB and the phosphorylation of Janus family kinase 1 (JAK1) were attenuated upon 25(OH)D(3) treatment. These data may provide an explanation for the therapeutic benefits and anti-inflammatory effects of 25(OH)D(3). Our findings should have important implications for the clinical therapy of diabetic periodontitis.
journal_name
Steroidsjournal_title
Steroidsauthors
Li H,Xie H,Fu M,Li W,Guo B,Ding Y,Wang Qdoi
10.1016/j.steroids.2012.10.015subject
Has Abstractpub_date
2013-02-01 00:00:00pages
115-20issue
2eissn
0039-128Xissn
1878-5867pii
S0039-128X(12)00291-7journal_volume
78pub_type
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