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KMID : 0829220100340040167
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Korean Journal of Oral and Maxillofacial Pathology
2010 Volume.34 No. 4 p.167 ~ p.177
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Analysis of Inflammatory Cytokines by Exposure of Hyperbaric Oxygen on P.gingivalis LPS Treated Human Gingival Fibroblast
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Lim Won-Bong
Won Jae-Woong
Kim In-Ae
Kim Ji-Sun
Ko Young-Jong
Kwon Hyuk-Il
Kim Sang-Woo
Li Xiaojie
KM Ahsan Kabir
Cha Hyun-Rok
Lim Dae-Young
Kim Seo-Yune
Choi Hong-Ran
Kim Ok-Joon
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Abstract
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Human gingival fibroblasts (hGFs) were reported to play an important role in inflammatory reactions to lipopolysaccharide (LPS) from P.gingivalis in the periodontal connective tissue. Although the biostimulatory effects of hyperbaric oxygen therapy, such as anti-inflammatory activity, have been reported, the pathological mechanism is not completely understood. This study examined the changes in the inflammatory cytokine profiles, which are produced after exposure to hyperbaric oxygen in P.gingivalis LPS-treated human gingival fibroblasts, and subsequently to examine the mitogen activated protein kinase (MAPK) pathway involved in cytokine production. Gingival fibroblasts with or without P.gingivalis LPS were exposed to hyperbaric oxygen, and the cytokine profiles in the supernatant were observed using a human inflammation antibody array. The expression of cyclooxyginase-2 (COX-2) protein, phosphorylation of extracellular signal-regulated kinase (ERK1/2), p38, and c-Jun-N-terminal kinase (JNK) MAPK by western blot analysis, and the amount of prostaglandin E2 (PGE2) in the supernatant by an enzyme-linked immunoassay were determined. COX-2 protein expression and PGE2productionwereincreasedsignificantlyintheP. gingivalis LPS-treated group, and were decreased by treating P. gingivalis LPS with hyperbaric oxygen. Treatment of P. gingivalis LPS in the gingival fibroblasts led an increase in the amount of pro-inflammatory-related cytokines interleukin-6 (IL-6) and IL-8 released, whereas hyperbaric oxygen inhibits the irrelease. Ananalysis of the MAPK signal transduction showed that hyperbaric oxygen induced a significant decrease in the level of P38 phosphorylation regardless of the presence or absence of LPS. In addition, hyperbaric oxygen promoted JNK phosphorylation, significantly in the presence of LPS. Hyperbaric oxygen can inhibit pro-inflammatory cytokines and mediate the MAPK signal pathway, and appears to be useful as an anti-inflammatory tool.
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KEYWORD
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Hyperbaric oxygen, Inflammation, Cytokine
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