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We aimed to characterize the H2B acetylation response to ICH, test the functional significance of modeled H2BK109 states, and identify a downstream effector of H2BK109Q\u2010mediated protection.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Pan\u2010H2B acetylation was examined in mice with collagenase\u2010induced ICH and in hemoglobin\u2010treated HT22 cells, and the histone acetylome of the mouse brain was profiled. H2BK109Q and H2BK109R were used to model acetylation\u2010mimetic and non\u2010acetylated lysine\u2010like states. Injury outcomes, axon\u2013myelin integrity, molecular profiles, and regional Galc knockdown were assessed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>ICH and hemoglobin reduced pan\u2010H2B acetylation, and acetylome profiling indicated reduced H2BK109ac. H2BK109Q\u2010expressing mice showed higher pan\u2010H2B acetylation, smaller hematomas, less edema and apoptosis, improved neurological function, and greater preservation of LFB, MBP, NF200, and axon\u2013myelin ultrastructure. Under matched hemoglobin exposure, H2BK109Q\u2010expressing HT22 cells showed higher BCL2\/BAX ratios and lower TUNEL positivity than H2BK109R\u2010expressing cells. In\u00a0vitro analyses highlighted GALC as a candidate downstream effector of H2BK109Q\u2010associated protection. In H2BK109Q\u2010expressing mice, Galc knockdown reduced LFB\u2010 and MBP\u2010positive areas and NF200 signals in the caudate putamen and corpus callosum compared with untreated and siNC controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>H2BK109Q attenuates acute ICH injury and preserves axon\u2013myelin integrity, with GALC contributing to these protective effects.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.71172","type":"journal-article","created":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T07:21:05Z","timestamp":1791530465000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Acetylation\u2010like\n                    <scp>H2BK109Q<\/scp>\n                    attenuates acute brain injury and preserves axon\u2010myelin integrity after intracerebral hemorrhage"],"prefix":"10.1002","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3278-3698","authenticated-orcid":false,"given":"Sinan","family":"Jin","sequence":"first","affiliation":[{"name":"Department of Pathology The First Affiliated Hospital of Harbin Medical University  Harbin China"},{"name":"State Key Laboratory of Frigid Zone Cardiovascular Disease  Harbin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meng","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Pathology The First Affiliated Hospital of Harbin Medical University  Harbin China"},{"name":"State Key Laboratory of Frigid Zone Cardiovascular Disease  Harbin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jincheng","family":"Meng","sequence":"additional","affiliation":[{"name":"Department of Pathology The First Affiliated Hospital of Harbin Medical University  Harbin China"},{"name":"State Key Laboratory of Frigid Zone 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