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- W2890121743 abstract "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.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.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.These results suggest that activation of STAT3 signaling attenuates ICH-induced neurogenesis and may delay neural recovery following hemorrhagic cerebral injury." @default.
- W2890121743 created "2018-09-27" @default.
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- W2890121743 date "2018-01-01" @default.
- W2890121743 modified "2023-09-24" @default.
- W2890121743 title "Activation of signal transducer and activator of transcription 3 signaling attenuates neurogenesis in a rat model of intracerebral hemorrhage" @default.
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- W2890121743 doi "https://doi.org/10.5137/1019-5149.jtn.23665-18.3" @default.
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