Intracerebral hemorrhage (ICH) is classified as a subtype of stroke and calcium (Ca) overload is a catalyst for ICH. This study explored the mechanisms of (signal transducer and activator of transcription 1) in the neuronal Ca overload after ICH. ICH mouse models and in vitro cell models were established. Stat1 and transient receptor potential melastatin 7 () were detected upregulated in ICH models. Afterward, the mice were infected with the lentivirus containing sh-Stat1, and HT22 cells were treated with si-Stat1 and the lentivirus containing pcDNA3.1-. The neurological functional impairment, histopathological damage, and Nissl bodies in mice were all measured. HT22 cell viability and apoptosis were identified. The levels of Ca, mRNA, H3K27 acetylation (H3K27ac), CaMKII-α, and p-Stat1 protein in the tissues and cells were determined. We found that silencing Stat1 alleviated ICH damage and repressed the neuronal Ca overload after ICH. H3K27ac enrichment in the promoter region was examined and we found that p-Stat1 accelerated transcription via promoting H3K27ac in the promoter region. Besides, overexpression increased Ca overload and aggravated ICH. Overall, p-Stat1 promoted transcription and further aggravated the Ca overload after ICH. We found Stat1 promotes transcription by promoting H3K27 acetylation and thus promotes calcium overload of neurons after intracerebral hemorrhage.
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