Turkish Neurosurgery
Activation of signal transducer and activator of transcription 3 signaling attenuates neurogenesis in a rat model of intracerebral hemorrhage
Li Haitao3, Huajun Zhou 1
1China Three Gorges University, Institute of Neurology, Yichang,
2China Three Gorges University, Department of Neurology, The First College of Clinical Medical Sciences, Yichang,
3China Three Gorges University, Department of radiology, The First College of Clinical Medical Sciences, Yichang,
DOI: 10.5137/1019-5149.JTN.23665-18.3

Aim:Neurogenesis plays an important role in promoting neurologic function after intracerebral hemorrhage (ICH). Signal transducer and activator of transcription 3 (STAT3) activation has been reported to negatively regulate neurogenesis. Previous studies have also demonstrated that activation of STAT3 signaling exerted a detrimental effect on ICH. In this study, we investigated the effect of STAT3 signaling on neurogenesis following ICH.Material and Methods:A rat model of ICH was induced via the stereotaxic injection of 100 µL autologous blood into the right globus pallidus. AG490 (0.25 mg/kg) was injected into the lateral ventricle after ICH to block STAT3 signaling. Brains were perfused to identify proliferating cell nuclear antigen (PCNA)+/ doublecortin (DCX) + nuclei by immunohistochemistry. In addition, the distribution and expression of phosphorylated STAT3 [p-STAT3 (Tyr705)] were evaluated by immunohistochemistry and western blot, respectively.Results:An enhanced level of p-STAT3 (Tyr705) was observed in neurons in the perihematomal region. An increase in DCX-positive cells and PCNA+/DCX+ nuclei was detected after ICH. Blocking STAT3 signaling with AG490 further increased the numbers of DCX-positive cells and PCNA+/DCX+ nuclei after ICH.Conclusion:These results suggest that activation of STAT3 signaling attenuates ICH-induced neurogenesis and may delay neural recovery following hemorrhagic cerebral injury.

Corresponding author : Li Haitao