Issue release date: 12.11.2024
2China Three Gorges University, Institute of Neurology, Yichang, Hubei, P. R. China
3China Three Gorges University, The First College of Clinical Medical Sciences, Department of Neurology, Yichang, Hubei, P. R. China DOI : 10.5137/1019-5149.JTN.23665-18.1 AIM: To investigate the effect of signal transducer and activator of transcription 3 (STAT3) signaling on neurogenesis following intracerebral hemorrhage (ICH).
MATERIAL and METHODS: A rat model of ICH was induced via the stereotaxic injection of 100 ?L 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 DCXpositive 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.
Keywords : Intracerebral hemorrhage, Neurogenesis, Signal transducer and activator of transcription 3, Rat