title: d-Allose Attenuates Overexpression of Inflammatory Cytokines after Cerebral Ischemia/Reperfusion Injury in Gerbil.
abstract: BACKGROUND
  The present study investigates the effects of d-allose, a rare sugar, on the inflammatory response after transient forebrain ischemia in the gerbil and whether it reduces oxidative stress (8-hydroxyl-2'-deoxyguanosine levels) and behavioral deficits.
  
  
  METHODS
  Transient forebrain ischemia was induced by occlusion of the bilateral common carotid arteries for 5 minutes. d-Allose was intraperitoneally injected immediately after ischemia (400 mg/kg). Inflammatory cytokines and oxidative damage in the hippocampus and behavioral deficits were examined 3 days after ischemia.
  
  
  RESULTS
  d-Allose administration reduced ischemia-induced cytokine production, oxidative stress, and behavioral deficits (motor and memory related).
  
  
  CONCLUSIONS
  The present results suggest that d-allose reduces brain injury after transient global ischemia by suppressing inflammation as well as by inhibiting oxidative stress.
authors.affiliation: Emergency Medical Center, Kagawa University Hospital, Miki, Japan.
authors.forename: Natsuyo
authors.initials: N
authors.lastname: Shinohara
authors.affiliation: Department of Medical Technology, Kagawa Prefectural University of Health Sciences, Takamatsu, Japan. Electronic address: tanakamu@kms.ac.jp.
authors.forename: Takehiro
authors.initials: T
authors.lastname: Nakamura
authors.affiliation: Emergency Medical Center, Kagawa University Hospital, Miki, Japan.
authors.forename: Yuko
authors.initials: Y
authors.lastname: Abe
authors.affiliation: Emergency Medical Center, Kagawa University Hospital, Miki, Japan.
authors.forename: Toru
authors.initials: T
authors.lastname: Hifumi
authors.affiliation: Emergency Medical Center, Kagawa University Hospital, Miki, Japan.
authors.forename: Kenya
authors.initials: K
authors.lastname: Kawakita
authors.affiliation: Department of Neurological Surgery, Kagawa University Faculty of Medicine, Miki, Japan.
authors.forename: Aya
authors.initials: A
authors.lastname: Shinomiya
authors.affiliation: Department of Neurological Surgery, Kagawa University Faculty of Medicine, Miki, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Tamiya
authors.affiliation: Department of Cell Physiology, Kagawa University Faculty of Medicine, Miki, Japan.
authors.forename: Masaaki
authors.initials: M
authors.lastname: Tokuda
authors.affiliation: Department of Neurosurgery, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Richard F
authors.initials: RF
authors.lastname: Keep
authors.affiliation: Department of Molecular Neurobiology, Kagawa University Faculty of Medicine, Miki, Japan.
authors.forename: Tohru
authors.initials: T
authors.lastname: Yamamoto
authors.affiliation: Emergency Medical Center, Kagawa University Hospital, Miki, Japan.
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Kuroda
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism*; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects*; D005849:Gerbillinae; D005947:Glucose / Q000627:therapeutic use*; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D009069:Movement Disorders / Q000188:drug therapy / Q000209:etiology; D015427:Reperfusion Injury / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism*; D013549:Sweetening Agents / Q000627:therapeutic use*; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D016207:Cytokines; D013549:Sweetening Agents; C002055:allose; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine; D005947:Glucose
keywords: Ischemia; cytokines; d-allose; hyperactivity; inflammation; oxidation; reperfusion