Papers

Peer-reviewed International journal
Aug 1, 2007

Decreased focal inflammatory response by G-CSF may improve stroke outcome after transient middle cerebral artery occlusion in rats.

Journal of neuroscience research
  • Yoshihide Sehara
  • ,
  • Takeshi Hayashi
  • ,
  • Kentaro Deguchi
  • ,
  • Hanzhe Zhang
  • ,
  • Atsushi Tsuchiya
  • ,
  • Toru Yamashita
  • ,
  • Violeta Lukic
  • ,
  • Makiko Nagai
  • ,
  • Tatsushi Kamiya
  • ,
  • Koji Abe

Volume
85
Number
10
First page
2167
Last page
74
Language
English
Publishing type
Research paper (scientific journal)

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.

Link information
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/17497673
ID information
  • ISSN : 0360-4012
  • Pubmed ID : 17497673

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