title: Treatment with resveratrol attenuates sublesional bone loss in spinal cord-injured rats.
abstract: OBJECTIVE
  Sublesional osteoporosis predisposes individuals with spinal cord injury (SCI) to an increased risk of low-trauma fracture. The aim of the present work was to investigate the effect of treatment with resveratrol (RES) on sublesional bone loss in spinal cord-injured rats.
  
  
  METHODS
  Complete SCI was generated by surgical transaction of the cord at the T10-12 level. Treatment with RES (400 mg·kg(-1) body mass per day(-1) , intragastrically) was initiated 12 h after the surgery for 10 days. Then, blood was collected and femurs and tibiae were removed for evaluation of the effects of RES on bone tissue after SCI.
  
  
  RESULTS
  Treatment of SCI rats with RES prevented the reduction of bone mass including bone mineral content and bone mineral density in tibiae, preserved bone structure including trabecular bone volume fraction, trabecular number, and trabecular thickness in tibiae, and preserved mechanical strength including ultimate load, stiffness, and energy in femurs. Treatment of SCI rats with RES enhanced femoral total sulfhydryl content, reduced femoral malondialdehyde and IL-6 mRNA levels. Treatment of SCI rats with RES suppressed the up-regulation of mRNA levels of PPARγ, adipose-specific fatty-acid-binding protein and lipoprotein lipase, and restored mRNA levels of Wnt1, low-density lipoprotein-related protein 5, Axin2, ctnnb1, insulin-like growth factor 1 (IGF-1) and receptor for IGF-1 in femurs and tibiae.
  
  
  CONCLUSIONS
  Treatment with RES attenuated sublesional bone loss in spinal-cord-injured rats, associated with abating oxidative stress, attenuating inflammation, depressing PPARγ signalling, and restoring Wnt/β-catenin and IGF-1 signalling.
authors.affiliation: Department of Orthopedics, The First Affiliated Hospital of the General Hospital of CPLA, Beijing, China.
authors.forename: Hua-Dong
authors.initials: HD
authors.lastname: Wang
authors.forename: Ya-Min
authors.initials: YM
authors.lastname: Shi
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Ji-Dong
authors.initials: JD
authors.lastname: Guo
authors.forename: Yu-Peng
authors.initials: YP
authors.lastname: Zhang
authors.forename: Shu-Xun
authors.initials: SX
authors.lastname: Hou
mesh_terms: D000818:Animals; D015519:Bone Density / Q000187:drug effects; D050071:Bone Density Conservation Agents / Q000494:pharmacology*; D004195:Disease Models, Animal; D005269:Femur / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000378:metabolism; D005786:Gene Expression Regulation; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D010024:Osteoporosis / Q000000981:diagnostic imaging / Q000209:etiology / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D018384:Oxidative Stress / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D011859:Radiography; D051381:Rats; D017207:Rats, Sprague-Dawley; D000077185:Resveratrol; D015398:Signal Transduction / Q000187:drug effects; D013119:Spinal Cord Injuries / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D013267:Stilbenes / Q000494:pharmacology*; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013977:Tibia / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000378:metabolism
chemical_list: D050071:Bone Density Conservation Agents; D018836:Inflammation Mediators; D012333:RNA, Messenger; D013267:Stilbenes; D013438:Sulfhydryl Compounds; D008315:Malondialdehyde; D000077185:Resveratrol
keywords: IGF-1; PPARγ; Wnt/β-catenin; inflammation; oxidative stress; resveratrol; spinal cord injury; sublesional bone loss