title: Activation of NF-κB pathway in oral buccal mucosa during small intestinal ischemia-reperfusion injury.
abstract: BACKGROUND
  Intestinal ischemia-reperfusion injury induces intestinal mucosal barrier disruption, systemic inflammatory response syndrome, multiorgan failure, and death. The major pathway for the systemic inflammatory responses depends on nuclear factor kappa B (NF-κB). However, direct measuring of NF-κB in injured tissues is not routinely available. Our aim was to determine whether NF-кB pathway in buccal mucosa is activated during intestinal ischemia-reperfusion injury.
  
  
  METHODS
  Male Sprague-Dawley rats were prepared for the animal experiment. Superior mesenteric artery (SMA) was exposed and clamped for 30 min in the intestinal ischemia-reperfusion (IR) group. SMA was exposed only in control group. Serum, buccal mucosa, and small intestinal mucosa were harvested in 90 min after reperfusion in IR or 120 min after SMA exposure in control group. Serum cytokine levels and tissue NF-κB pathway activities were measured.
  
  
  RESULTS
  Serum TNF-α (5.49 ± 2.72 versus 1.77 ± 1.20 pg/mL, P = 0.002) and interleukin-6 (232.32 ± 29.98 versus 115.92 ± 17.81 pg/mL, P = 0.002) levels were significantly higher in IR than control group. Intestinal mucosal cytoplasmic phosphorylated inhibitor kappa B (IκB)/IκB ratio, nuclear NF-κB expression, and NF-κB DNA-binding activity were significantly higher in IR than control group. Buccal mucosal cytoplasmic phosphorylated IκB/IκB ratio, nuclear NF-κB expression, and NF-κB DNA-binding activity were also higher in IR than control group.
  
  
  CONCLUSIONS
  Buccal mucosal NF-κB pathway was activated by intestinal ischemia-reperfusion injury. The present study suggests that buccal mucosal may be considered as an indicator for the assessment of intestinal ischemia-reperfusion injury.
authors.affiliation: Department of Oral and Maxillofacial Surgery, School of Dentistry and Institute of Oral Bioscience, Brain Korea 21 Project, Chonbuk National University, Chonju, Chonbuk, Korea.
authors.forename: Seong-Il
authors.initials: SI
authors.lastname: Kim
authors.forename: Young-Bin
authors.initials: YB
authors.lastname: Kim
authors.forename: Kwang-Moo
authors.initials: KM
authors.lastname: Koh
authors.forename: Yeo-Kyu
authors.initials: YK
authors.lastname: Youn
authors.forename: Gil-Joon
authors.initials: GJ
authors.lastname: Suh
authors.forename: Eui-Sic
authors.initials: ES
authors.lastname: Cho
authors.forename: Dae-Ho
authors.initials: DH
authors.lastname: Leem
authors.forename: Jin-A
authors.initials: JA
authors.lastname: Baek
authors.forename: Hyo-Keun
authors.initials: HK
authors.lastname: Shin
authors.forename: Seung-O
authors.initials: SO
authors.lastname: Ko
mesh_terms: D000818:Animals; D015850:Interleukin-6 / Q000097:blood; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology; D007421:Intestine, Small / Q000098:blood supply* / Q000378:metabolism* / Q000473:pathology; D008297:Male; D023421:Models, Animal; D009061:Mouth Mucosa / Q000378:metabolism* / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology; D015203:Reproducibility of Results; D012720:Severity of Illness Index; D015398:Signal Transduction / Q000502:physiology*; D051996:Transcription Factor RelA / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015850:Interleukin-6; D016328:NF-kappa B; C498145:Rela protein, rat; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha