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• W2079394559 abstract "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 μg/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‐α (TNF‐α) at 8–72 hr, transforming growth factor‐β (TGF‐β) 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. © 2007 Wiley‐Liss, Inc." @default.
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• W2079394559 date "2007-05-11" @default.
• W2079394559 modified "2023-10-13" @default.
• W2079394559 title "Decreased focal inflammatory response by G-CSF may improve stroke outcome after transient middle cerebral artery occlusion in rats" @default.
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• W2079394559 doi "https://doi.org/10.1002/jnr.21341" @default.
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