Introduction:
This study aimed to determine the relationship between granulocyte colony-stimulating factor (G-CSF) and the Notch signaling pathway in ischemic brain injury.

Material and methods:
PC-12 cells were treated with nerve growth factor (NGF) to induce neuronal differentiation and were then divided into seven groups: 1) no treatment (control); 2) oxygen-glucose deprivation (OGD) model; 3) overexpressed granulocyte colony-stimulating factor (G-CSF) + OGD model; 4) transfected empty vector (negative control – NC) + OGD model; 5) overexpressed G-CSF + γ-secretase inhibitor MW167 + OGD model; 6) MW167 + OGD model; and 7) NC + MW167 + OGD model. The cells were analyzed using immunohistochemistry, apoptosis, and CCK8 assays. The expression of the related molecules in the Notch pathway was detected using Western blotting and quantitative PCR (Q-PCR).

Results:
Most of the PC-12 cells were neuron-specific enolase (NSE)-positive after administering the NGF treatment. When compared with the control group, the MW167 + OGD and NC + MW167 + OGD groups had the lowest optical density (OD) values, followed by the OGD, NC + OGD, and the G-CSF + MW167 + OGD groups. The G-CSF + OGD group had the highest OD value. Concerning apoptosis detection, the control group had the lowest apoptosis rate. The highest apoptosis rates were found in the MW167 + OGD, the OGD, and then the G-CSF + OGD groups.

Conclusions:
Blocking of the Notch pathway can attenuate the granulocyte colony-stimulating factor (G-CSF) effects, whereas G-CSF overexpression can activate the Notch pathway to resist the effects of oxygen-glucose deprivation.