title: Role of transcription factors in small intestinal ischemia-reperfusion injury and tolerance induced by ischemic preconditioning.
abstract: BACKGROUND
  Small intestinal ischemia-reperfusion (I/R) injury, a clinically important condition, induces severe organ damage. Ischemic preconditioning (IPC) produces tolerance to long-term I/R by inducing a short-term I/R. Herein, we have examined the reduction in the extent of injury by IPC.
  
  
  METHODS
  Small intestinal I/R injury was induced in rats by clamping the superior mesenteric artery (SMA) for 30 minutes followed by reperfusion for various 30 minutes. The IPC + I/R group underwent a short-term I/R (IPC) prior to long-term I/R. Nuclear factor-κB (NF-κB) activity was analyzed by an electrophoretic mobility shift assay and cytokine mRNA levels, by reverse transcription-polymerase chain reaction. Apoptosis-related genes were analyzed by Western blotting and immunohistochemistry, and apoptotic cells, by TUNEL staining.
  
  
  RESULTS
  The animals were subjected to 30 minutes of ischemia followed by 30 minutes of reperfusion. NF-κB activity increased in the I/R group and decreased in the IPC + I/R group. The IPC + I/R group showed decreased cytokine in mRNA levels. Expression of the proapoptotic gene caspase-3 was increased in the I/R and decreased in the IPC + I/R group. Expression of the antiapoptotic gene Bcl-xL was increased in the IPC + I/R group. The number of apoptotic cells was increased in the I/R and decreased in the IPC + I/R group.
  
  
  CONCLUSIONS
  Small intestinal I/R injury was reduced by IPC produced by clamping the SMA; thus, IPC may have potential clinical applications in the future.
authors.affiliation: Department of Gastroenterologic Surgery, Division of Cancer Medicine, Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Takeshita
authors.forename: T
authors.initials: T
authors.lastname: Tani
authors.forename: S
authors.initials: S
authors.lastname: Harada
authors.forename: H
authors.initials: H
authors.lastname: Hayashi
authors.forename: H
authors.initials: H
authors.lastname: Itoh
authors.forename: H
authors.initials: H
authors.lastname: Tajima
authors.forename: I
authors.initials: I
authors.lastname: Ohnishi
authors.forename: H
authors.initials: H
authors.lastname: Takamura
authors.forename: S
authors.initials: S
authors.lastname: Fushida
authors.forename: M
authors.initials: M
authors.lastname: Kayahara
mesh_terms: D000818:Animals; D017209:Apoptosis; D001665:Binding Sites; D015153:Blotting, Western; D053148:Caspase 3 / Q000378:metabolism; D003250:Constriction; D004247:DNA / Q000378:metabolism; D004195:Disease Models, Animal; D024202:Electrophoretic Mobility Shift Assay; D005786:Gene Expression Regulation; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics; D053583:Interleukin-1beta / Q000235:genetics; D019194:Ischemic Preconditioning; D007583:Jejunum / Q000098:blood supply* / Q000378:metabolism* / Q000473:pathology; D008297:Male; D017538:Mesenteric Artery, Superior / Q000601:surgery; D016328:NF-kappa B / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D051020:bcl-X Protein / Q000378:metabolism
chemical_list: C494813:Bcl2l1 protein, rat; D053583:Interleukin-1beta; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D051020:bcl-X Protein; D018799:Intercellular Adhesion Molecule-1; D004247:DNA; C505410:Casp3 protein, rat; D053148:Caspase 3