title: Transient lack of glucose but not O2 is involved in ischemic postconditioning-induced neuroprotection.
abstract: OBJECTIVE
  Cerebral ischemic postconditioning has emerged recently as a kind of endogenous strategy for neuroprotection. We set out to test whether hypoxia or glucose deprivation (GD) would substitute for ischemia in postconditioning.
  
  
  METHODS
  Adult male C57BL/6J mice were treated with postconditioning evoked by ischemia (bilateral common carotid arteries occlusion) or hypoxia (8% O(2) ) after 45-min middle cerebral arterial occlusion. Corticostriatal slices from mice were subjected to 1-min oxygen-glucose deprivation (OGD), GD, or oxygen deprivation (OD) postconditioning at 5 min after 15-min OGD.
  
  
  RESULTS
  Hypoxic postconditioning did not decrease infarct volume or improve neurologic function at 24 h after reperfusion, while ischemic postconditioning did. Similarly, OGD and GD but not OD postconditioning attenuated the OGD/reperfusion-induced injury in corticostriatal slices. The effective duration of low-glucose (1 mmol/L) postconditioning was longer than that of OGD postconditioning. Moreover, OGD and GD but not OD postconditioning reversed the changes of glutamate, GABA, glutamate transporter-1 protein expression, and glutamine synthetase activity induced by OGD/reperfusion.
  
  
  CONCLUSIONS
  These results suggest that the transient lack of glucose but not oxygen plays a key role in ischemic postconditioning-induced neuroprotection, at least partly by regulating glutamate metabolism. Low-glucose postconditioning might be a clinically safe and feasible therapeutic approach against cerebral ischemia/reperfusion injury.
authors.affiliation: Department of Pharmacology, Shanxi Medical University, Taiyuan, China.
authors.forename: Yan-Ying
authors.initials: YY
authors.lastname: Fan
authors.forename: Xiang-Nan
authors.initials: XN
authors.lastname: Zhang
authors.forename: Ping
authors.initials: P
authors.lastname: He
authors.forename: Zhe
authors.initials: Z
authors.lastname: Shen
authors.forename: Yao
authors.initials: Y
authors.lastname: Shen
authors.forename: Xiao-Fen
authors.initials: XF
authors.lastname: Wang
authors.forename: Wei-Wei
authors.initials: WW
authors.lastname: Hu
authors.forename: Zhong
authors.initials: Z
authors.lastname: Chen
mesh_terms: D000818:Animals; D020520:Brain Infarction / Q000209:etiology* / Q000517:prevention & control*; D002851:Chromatography, High Pressure Liquid; D004195:Disease Models, Animal; D005947:Glucose / Q000172:deficiency*; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D000860:Hypoxia / Q000150:complications* / Q000473:pathology; D066298:In Vitro Techniques; D020244:Infarction, Middle Cerebral Artery / Q000150:complications*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015424:Reperfusion / Q000379:methods*; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D005974:Glutamate-Ammonia Ligase; D005947:Glucose