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.

I. Introduction
 II. Material and Method
  1. Cell culture and chemicals
  2. Hyperbaric oxygen treatment
  3. Cell viability
  4. Western blot analysis
  5. Enzyme-Linked Immunosorbent assay for PGE2
  6. Cytokine profiling
  7. Statistical analysis
 III. Results
  1. Effects of hyperbaric oxygen on cell viability
  2. The effect of hyperbaric oxygen on P. gingivalisLPS-induced COX-2 expression and PGE2production
  3. The effect of hyperbaric oxygen on cytokineproduction
  4. The effect of hyperbaric oxygen on mitogenactivatedprotein kinase (MAPK)phosphorylation in hGFs
 IV. Discussion
 V. Reference

• 임원봉(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University, These authors contributed equally to this work) | Won Bong Lim
• 원재웅(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University, These authors contributed equally to this work) | Jae Woong Won
• 김인애(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University) | In Ae Kim
• 김지선(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University) | Ji Sun Kim
• 고영종(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University) | Young Jong Ko
• 권혁일(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University) | Hyuk Il Kwon
• 김상우(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University) | Sang Woo Kim
• Li Xiaojie(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University)
• KM Ahsan Kabir(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University)
• 차현록(KITECH) | Hyun Rok Cha
• 임대영(KITECH) | Dae Young Lim
• 김서연(Department of Dental Hygiene, Songwon College University) | Seo Yune Kim
• 최홍란(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University) | Hong Ran Choi
• 김옥준(Dental Research Institute, Department of Oral Pathology, School of Dentistry, Chonnam National University) | Ok Joon Kim correspondence