title: 25-hydroxyvitamin D3 ameliorates periodontitis by modulating the expression of inflammation-associated factors in diabetic mice.
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.
authors.affiliation: State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, PR China.
authors.forename: Hao
authors.initials: H
authors.lastname: Li
authors.forename: Honghui
authors.initials: H
authors.lastname: Xie
authors.forename: Min
authors.initials: M
authors.lastname: Fu
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Bin
authors.initials: B
authors.lastname: Guo
authors.forename: Yi
authors.initials: Y
authors.lastname: Ding
authors.forename: Qi
authors.initials: Q
authors.lastname: Wang
mesh_terms: D016301:Alveolar Bone Loss / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000473:pathology; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002112:Calcifediol / Q000494:pharmacology / Q000627:therapeutic use*; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000150:complications* / Q000188:drug therapy* / Q000201:enzymology; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005215:Fasting / Q000097:blood; D005881:Gingiva / Q000473:pathology; D007249:Inflammation / Q000097:blood / Q000150:complications* / Q000188:drug therapy; D053613:Janus Kinase 1 / Q000378:metabolism; D008297:Male; D008336:Mandibular Diseases / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism; D010518:Periodontitis / Q000097:blood / Q000150:complications* / Q000188:drug therapy* / Q000473:pathology; D054578:Protein Tyrosine Phosphatase, Non-Receptor Type 2 / Q000378:metabolism; D018167:Receptors, Calcitriol / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D001786:Blood Glucose; D016328:NF-kappa B; D018167:Receptors, Calcitriol; D014409:Tumor Necrosis Factor-alpha; D053613:Janus Kinase 1; D054578:Protein Tyrosine Phosphatase, Non-Receptor Type 2; C516653:Ptpn2 protein, mouse; D002112:Calcifediol