title: Lithium pretreatment reduces brain injury after intracerebral hemorrhage in rats.
abstract: OBJECTIVE
  In addition to the mood-stabilizing effects of lithium in patients with bipolar disorder, recent in vitro and in vivo studies in rodents increasingly implicate that lithium may be useful for treating acute cerebral ischemia, neuroinflammatory conditions,  and chronic neurodegenerative diseases. However, whether lithium has a protective effect against hemorrhagic stroke is yet unknown. To test this possibility, we attempted to determine lithium's effect on experimental intracerebral hemorrhage (ICH).
  
  
  METHODS
  We treated adult  rats with either lithium (2 mEq/kg) or saline for 3 days before inducing ICH via a stereotaxic infusion of collagenase into the left basal ganglia. Hematoma volumes, hemispheric swelling, long-term hemispheric atrophy, microglial activation, cell death, cyclooxygenase-2 expression, and behavioral  outcomes were assessed.
  
  
  RESULTS
  Per behavioral tests 2 days after ICH, the lithium-treated group recovered better than did the saline-treated group. Three days after ICH, the hematoma volumes did not differ between the groups, but hemispheric swelling was less in the lithium-treated  group. Forty-two days after ICH, hemispheric atrophy was less in the lithium-treated group. Lithium reduced cell death, cyclooxygenase-2 expression, and reactive microglia in the perihematomal regions.
  
  
  CONCLUSIONS
  The present study shows that lithium, via anti-inflammation, reduces  the perihematomal cell death, which is associated with sensorimotor recovery after experimental ICH.
authors.affiliation: Eulji General Hospital, Seoul, Korea.
authors.forename: K
authors.initials: K
authors.lastname: Kang
authors.forename: Y-J
authors.initials: YJ
authors.lastname: Kim
authors.forename: Y-H
authors.initials: YH
authors.lastname: Kim
authors.forename: J N
authors.initials: JN
authors.lastname: Roh
authors.forename: J-M
authors.initials: JM
authors.lastname: Nam
authors.forename: P-Y
authors.initials: PY
authors.lastname: Kim
authors.forename: W-S
authors.initials: WS
authors.lastname: Ryu
authors.forename: S-H
authors.initials: SH
authors.lastname: Lee
authors.forename: B-W
authors.initials: BW
authors.lastname: Yoon
mesh_terms: D000818:Animals; D001929:Brain Edema / Q000209:etiology / Q000517:prevention & control; D001930:Brain Injuries / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D016923:Cell Death / Q000187:drug effects; D002543:Cerebral Hemorrhage / Q000139:chemically induced / Q000150:complications*; D024141:Collagen Type IV / Q000633:toxicity; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004195:Disease Models, Animal; D006406:Hematoma / Q000209:etiology / Q000473:pathology; D008094:Lithium / Q000008:administration & dosage*; D008297:Male; D018696:Neuroprotective Agents / Q000008:administration & dosage*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D016037:Single-Blind Method
chemical_list: D024141:Collagen Type IV; D018696:Neuroprotective Agents; D008094:Lithium; D009195:Peroxidase; D051546:Cyclooxygenase 2