Effect of 635 nm irradiation on high glucose-boosted inflammatory responses in LPS-induced MC3T3-E1 cells.
Hyperglycemia occurs in patients with poorly controlled diabetes mellitus and contributes to bone resorption and increased susceptibility to bacterial infections. Hyperglycemia can incite low-grade inflammation that can contribute to the resorption of bone, especially the periodontal bone. The increased susceptibility to periodontal infections can contribute to bone resorption through the activation of osteoclasts. In this study, the osteoblastic, clonal cell line, MC3T3-E1, was used in an in vitro model of hyperglycemia and lipopolysaccharide-induced reactive oxygen species generation to determine the potential anti-inflammatory effect of 635 nm light-emitting diode (LED) irradiation or whether 635 nm LED irradiation can be a potential anti-inflammatory treatment. LED irradiation of MC3T3-E1 cells stimulated with lipopolysaccharide in a high glucose-containing medium decreased the level of cyclooxygenase gene and protein expression and reduced the level of prostaglandin E2 expression by decreasing the amount of reactive oxygen species generation. LED irradiation also inhibited the osteoclastogenesis in MC3T3-E1 cells by regulating the receptor activator of nuclear factor kappa-B ligand and osteoprotegerin. These findings reveal the mechanisms which are important in the pathogenesis of diabetic periodontitis and highlight the beneficial effects of 635 nm LED irradiation in reducing the adverse effects of diabetic periodontitis.
Department of Oral Pathology, School of Dentistry, Dental Science Research Institute, Chonnam National University, Bug-Gu, Gwangju, 500-757, South Korea.
HyukIl
H
Kwon
WonBong
W
Lim
JiSun
J
Kim
SangMi
S
Jeon
SangWoo
S
Kim
Sandeep
S
Karna
HyunRok
H
Cha
OkJoon
O
Kim
HongRan
H
Choi
D016475:3T3 Cells; D000818:Animals; D051545:Cyclooxygenase 1 / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D015870:Gene Expression / Q000528:radiation effects; D005947:Glucose / Q000378:metabolism; D006943:Hyperglycemia / Q000150:complications / Q000378:metabolism / Q000473:pathology; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism; D008027:Light; D008070:Lipopolysaccharides / Q000494:pharmacology; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D010006:Osteoblasts / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects*; D053244:Osteoprotegerin / Q000235:genetics / Q000378:metabolism; D010789:Phototherapy; D053245:RANK Ligand / Q000235:genetics / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D053244:Osteoprotegerin; D053245:RANK Ligand; D017382:Reactive Oxygen Species; C506031:Tnfrsf11b protein, mouse; C505689:Tnfsf11 protein, mouse; C077623:Ptgs2 protein, mouse; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496512:Ptgs1 protein, mouse; D005947:Glucose; D015232:Dinoprostone