title: Ghrelin alleviates spinal cord injury in rats via its anti-inflammatory effects.
abstract: OBJECTIVE
  Spinal cord injury (SCI) leads to an inflammatory response that generates     substantial secondary damage within the tissue besides the primary damage.     Ghrelin, 28 amino-acid peptide, has been shown to modulate the release of     proinflammatory cytokines and exert antiinflammatory effects. The aim of the     current study was to investigate the anti-inflammatory effects of ghrelin, in a     rat model of SCI.
  
  
  METHODS
  Wistar albino rats were divided as     control, SCI, and ghrelin-treated (10 μg/kg/day, ip) SCI groups. In order     to induce SCI, a standard weight-drop method that induced a moderately severe     injury (100 g/cm force) at T10, was used. Injured animals were given either     ghrelin or saline 15 min post-injury.
  
  
  RESULTS
  In plasma samples,     neuron-specific enolase (NSE) and S-100β protein levels were evaluated.     Spinal cord samples were taken for histological examination or determination of     myeloperoxidase (MPO) activity and DNA fragmentation. SCI caused significant     increases in plasma NSE and S-100β levels and tissue MPO activity and DNA     damage. On the other hand, ghrelin treatment improved histological findings as     well as biochemical parameters while it failed to improve the impairment of the     neurological functions due to SCI.
  
  
  CONCLUSIONS
  The present study suggests that     ghrelin could reduce SCI-induced oxidative stress and exert anti-inflammatory     effects in the spinal cord following trauma.
authors.affiliation: Samsun Education and Research Hospital, Department of Neurosurgery, Samsun, Turkey.
authors.forename: Mehmet
authors.initials: M
authors.lastname: Erşahın
authors.forename: Hale Zerrin
authors.initials: HZ
authors.lastname: Toklu
authors.forename: Can
authors.initials: C
authors.lastname: Erzık
authors.forename: Dilek
authors.initials: D
authors.lastname: Akakin
authors.forename: Sermin
authors.initials: S
authors.lastname: Tetık
authors.forename: Göksel
authors.initials: G
authors.lastname: Sener
authors.forename: Berrak Cağlayan
authors.initials: BC
authors.lastname: Yeğen
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000378:metabolism / Q000494:pharmacology*; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology; D015415:Biomarkers / Q000378:metabolism; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects; D004195:Disease Models, Animal; D054439:Ghrelin / Q000378:metabolism / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000378:metabolism; D009187:Myelitis / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D009410:Nerve Degeneration / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D009414:Nerve Growth Factors / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000378:metabolism / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D010243:Paralysis / Q000188:drug therapy / Q000503:physiopathology; D009195:Peroxidase / Q000378:metabolism; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000378:metabolism; D013116:Spinal Cord / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D015415:Biomarkers; D016207:Cytokines; D054439:Ghrelin; D018836:Inflammation Mediators; D009414:Nerve Growth Factors; D018696:Neuroprotective Agents; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D009195:Peroxidase; D010751:Phosphopyruvate Hydratase