title: Ischemic preconditioning ameliorates intestinal injury induced by ischemia-reperfusion in rats.
abstract: OBJECTIVE
  To evaluate preventative effects of ischemic preconditioning (IP) in a rat model of intestinal injury induced by ischemia-reperfusion (IR).
  
  
  METHODS
  Male Sprague-Dawley rats (250-300 g) were fasted for 24 h with free access to water prior to the operation. Eighteen rats were randomly divided into three experimental groups: S group (n = 6), rats were subjected to isolation of the superior mesenteric artery (SMA) for 40 min, then the abdomen was closed; IR group (n = 6), rats were subjected to clamping the SMA 40 min, and the abdomen was closed followed by a 4-h reperfusion; IP group (n = 6) rats underwent three cycles of 5 min ischemia and 5 min reperfusion, then clamping of the SMA for 40 min, then the abdomen was closed and a 4-h reperfusion followed. All animals were euthanized by barbiturate overdose (150 mg/kg pentobarbital sodium, i.v.) for tissue collection, and the SMA was isolated via median abdominal incision. Intestinal histologic injury was observed. Malondialdehyde (MDA), myeloperoxidase (MPO) and tumor necrosis factor (TNF)-α concentrations in intestinal tissue were measured. Intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 expression, as well as nuclear factor (NF)-κB activity and expression in intestinal tissue were also determined.
  
  
  RESULTS
  Compared with the IR group, IP reduced IR-induced histologic injury of the intestine in rats (2.00 ± 0.71 vs 3.60 ± 0.84, P < 0.05). IP significantly inhibited the increase in MDA content (5.6 ± 0.15 μmol/L vs 6.84 ± 0.18 μmol/L, P < 0.01), MPO activity (0.13 ± 0.01 U/L vs 0.24 ± 0.01 U/L, P < 0.01), and TNF-α levels (7.79 ± 2.35 pg/mL vs 10.87 ± 2.48 pg/mL, P < 0.05) in the intestinal tissue of rats. IP also markedly ameliorated the increase in ICAM-1 (204.67 ± 53.27 vs 353.33 ± 45.19, P < 0.05) and VCAM-1 (256.67 ± 58.59 vs 377.33 ± 41.42, P < 0.05) protein expression in the intestinal tissues. Additionally, IP remarkably decreased NF-κB activity (0.48 ± 0.16 vs 0.76 ± 0.22, P < 0.05) and protein expression (320.23 ± 38.16 vs 520.76 ± 40.53, P < 0.01) in rat intestinal tissue.
  
  
  CONCLUSIONS
  IP may protect against IR-induced intestinal injury by attenuation of the neutrophil-endothelial adhesion cascade via reducing ICAM-1 and VCAM-1 expression and TNF-α-induced NF-κB signaling pathway activity.
authors.affiliation: Yuan-Yuan Ji, Scientific Research Centre, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
authors.forename: Yuan-Yuan
authors.initials: YY
authors.lastname: Ji
authors.affiliation: Yuan-Yuan Ji, Scientific Research Centre, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
authors.forename: Zhi-Dong
authors.initials: ZD
authors.lastname: Wang
authors.affiliation: Yuan-Yuan Ji, Scientific Research Centre, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
authors.forename: Shu-Feng
authors.initials: SF
authors.lastname: Wang
authors.affiliation: Yuan-Yuan Ji, Scientific Research Centre, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
authors.forename: Bao-Tai
authors.initials: BT
authors.lastname: Wang
authors.affiliation: Yuan-Yuan Ji, Scientific Research Centre, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
authors.forename: Zheng-An
authors.initials: ZA
authors.lastname: Yang
authors.affiliation: Yuan-Yuan Ji, Scientific Research Centre, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
authors.forename: Xiao-Rong
authors.initials: XR
authors.lastname: Zhou
authors.affiliation: Yuan-Yuan Ji, Scientific Research Centre, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
authors.forename: Ni-Na
authors.initials: NN
authors.lastname: Lei
authors.affiliation: Yuan-Yuan Ji, Scientific Research Centre, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004, Shaanxi Province, China.
authors.forename: Wei-Na
authors.initials: WN
authors.lastname: Yue
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D003250:Constriction; D004195:Disease Models, Animal; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000098:blood supply* / Q000473:pathology; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D017538:Mesenteric Artery, Superior / Q000503:physiopathology; D065666:Mesenteric Ischemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D016328:NF-kappa B / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015398:Signal Transduction; D013152:Splanchnic Circulation; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D015415:Biomarkers; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde
keywords: Intercellular adhesion molecule; Ischemia-reperfusion; Ischemic preconditioning; Nuclear factor-κB; Tumor necrosis factor-α