title: Decreased focal inflammatory response by G-CSF may improve stroke outcome after transient middle cerebral artery occlusion in rats.
abstract: Recent studies have shown that administration of granulocyte colony-stimulating factor (G-CSF) is neuroprotective. However, the precise mechanisms of the neuroprotective effect of G-CSF are not entirely known. We carried out 90-min transient middle cerebral occlusion (tMCAO) of rats. The rats were injected with vehicle or G-CSF (50 mug/kg) immediately after reperfusion and sacrificed 8, 24, or 72 hr later. 2,3,5-Triphenyltetrazolium chloride (TTC) staining was carried out using brain sections of 72 hr, and immunohistochemistry was carried out with those of 8, 24, and 72 hr. TTC-staining showed a significant reduction of infarct volume in the G-CSF-treated group (**P < 0.01). Immunohistochemistry showed a significant decrease of the number of cells expressing tumor necrosis factor-alpha (TNF-alpha) at 8-72 hr, transforming growth factor-beta (TGF-beta) and inducible nitric oxide synthase (iNOS) at 24 and 72 hr after tMCAO in the peri-ischemic area (*P < 0.05 each). Our data suggest that the suppression of inflammatory cytokines and iNOS expression may be one mechanism of neuroprotection by G-CSF.
authors.affiliation: Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
authors.forename: Yoshihide
authors.initials: Y
authors.lastname: Sehara
authors.forename: Takeshi
authors.initials: T
authors.lastname: Hayashi
authors.forename: Kentaro
authors.initials: K
authors.lastname: Deguchi
authors.forename: Hanzhe
authors.initials: H
authors.lastname: Zhang
authors.forename: Atsushi
authors.initials: A
authors.lastname: Tsuchiya
authors.forename: Toru
authors.initials: T
authors.lastname: Yamashita
authors.forename: Violeta
authors.initials: V
authors.lastname: Lukic
authors.forename: Makiko
authors.initials: M
authors.lastname: Nagai
authors.forename: Tatsushi
authors.initials: T
authors.lastname: Kamiya
authors.forename: Koji
authors.initials: K
authors.lastname: Abe
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D007150:Immunohistochemistry; D020244:Infarction, Middle Cerebral Artery / Q000150:complications*; D007249:Inflammation / Q000209:etiology / Q000473:pathology*; D008297:Male; D009420:Nervous System / Q000503:physiopathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020521:Stroke / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D018696:Neuroprotective Agents; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D016179:Granulocyte Colony-Stimulating Factor; D052247:Nitric Oxide Synthase Type II