Abstract
Objective To investigate the effect of intranasal administration of recombinant human granulocyte colony stimulating factor (rhG-CSF) on Fas ligand (FasL) and hemeoxygenase-1 (HO-1) expressions in the cortical brain tissue of rats with ischemic cerebral infarction. Methods Sixty adult male SD rats were randomly assigned into 6 groups, namely the normal control group (n=6), sham-operated group (n=6), middle cerebral artery occlusion (MCAO) group (model group), and another 3 MCAO groups with intranasal administration of normal saline (NS), subcutaneous rhG-CSF injection, and intranasai rhG-CSF administration, respectively. In the 4 MCAO groups (n=12), the rats were subjected to temporary middle cerebral artery occlusion (MCAO) for 2 h, and on the next and third days following MCAO, 6 rats from each group were sacrificed and the coronal frozen sections of the brain tissue were prepared to detect the expressions of FasL and HO-1 in the ischemic penumbra using immunohistochernical staining. Laser scanning confocal microscopy was performed to observe the amount of positive cells in the ischemic penumbra. Results In both of the normal control and sham-operated groups, only a small number of FasL- and HO-l-positive cells were found in the brain of the rats (P>0.05). In MCAO model group, the expressions of FasL and HO-1 increased obviously, which were higher on day 1 than on day 3 and located mainly in the ischemic penumbra, and saline administration did not cause obvious changes in their expressions (P>0.05). rhG-CSF treatment, administered either intranasally or subcutaneously, resulted in significantly lowered FasL expression and increased HO-1 expression, but the changes were more obvious in intranasal rhG-CSF group (P<0.05). Conclusion Intranasal rhG-CSF administration offers brain protection by inhibiting FasL expression and up-regulating HO-1 expression in rats with cerebral ischemia. Key words: Cerebral ischcmia; Recombinant human granulocyte colony stimulating factor; Fas ligand; Hemeoxygenase-1; Intranasal pathway
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