title: [Protective effect of tacrolimus postconditioning on oxidative stress injury provoked by spinal cord ischemia-reperfusion in rats].
abstract: OBJECTIVE
  To investigate whether protective effect of tacrolimus postconditioning on rats' spinal cord ischemia-reperfusion injury is mediated by up-regulation of activity of endogenous antioxidant enzymes and down-regulation of production of oxygen free radicals.
  
  
  METHODS
  Ninety male Sprague-Dawley rats were randomly divided into ischemia-reperfusion (IR) group, tacrolimus postconditioning (TP) group and sham operation (SO) group. The model of spinal cord ischemia was prepared by means of catheterization through femoral artery and balloon dilatation. IR group underwent reperfusion 20 min after spinal cord ischemia. TP group experienced a single injection of tacrolimus (0.5 mg/kg) through the left common carotid artery at the onset of reperfusion. SO group received femoral artery catheterization only. Fluoro spectro photometry was employed to detect the level of reactive oxygen species (ROS) in injured spinal cord segment at 15 minutes after reperfusion. The content of malondialdehyde (MDA) and activity of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) were determined at 15 minutes, 1, 6, and 24 hours after reperfusion respectively. BBB scale was conducted to evaluate hindlimb motor function at 14 days after reperfusion.
  
  
  RESULTS
  The level of ROS in TP group was significantly lower than that in IR group at 15 minutes after reperfusion. The activity of SOD was significantly higher in TP group than in IR group at all observational time points, while the activities of CAT and GSH-PX were significantly higher in TP group than in IR group at 1 and 6 hours after reperfusion. The content of MDA in TP group was significantly less than that in IR group at all observational time points. The motor function score of TP group was significantly superior to that of IR group at 14 days after reperfusion.
  
  
  CONCLUSIONS
  Tacrolimus post conditioning can improve activity of endogenous antioxidant enzymes, decrease production of oxygen free radicals, suppress lipid peroxidation, and thereby promote functional recovery after spinal cord ischemia-reperfusion injury in rats.
authors.affiliation: Department of Spine Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China. Email: mountor@126.com.
authors.forename: Feng
authors.initials: F
authors.lastname: Pan
authors.forename: Yan-xiang
authors.initials: YX
authors.lastname: Cheng
authors.forename: Feng-hua
authors.initials: FH
authors.lastname: Tao
authors.forename: Cheng-liang
authors.initials: CL
authors.lastname: Zhu
authors.forename: Zhang-hua
authors.initials: ZH
authors.lastname: Li
authors.forename: Hai-ying
authors.initials: HY
authors.lastname: Tao
authors.forename: Bin
authors.initials: B
authors.lastname: He
authors.forename: Ling
authors.initials: L
authors.lastname: Yu
authors.forename: Yang
authors.initials: Y
authors.lastname: Liu
authors.forename: Huan
authors.initials: H
authors.lastname: Tang
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005979:Glutathione Peroxidase / Q000378:metabolism; D057775:Ischemic Postconditioning; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism*; D020760:Spinal Cord Ischemia / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism; D016559:Tacrolimus / Q000494:pharmacology*
chemical_list: D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D016559:Tacrolimus