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Knowledge about the influence of TMAO\u2010related inflammatory response on the pathological process of acute stroke is limited. This study was designed to explore the effects of TMAO on neuroinflammation, brain injury severity, and long\u2010term neurologic function in mice with acute intracerebral hemorrhage (ICH). We fed mice with either a regular chow diet or a chow diet supplemented with 1.2% choline pre\u2010 and post\u2010ICH. In this study, we measured serum levels of TMAO with ultrahigh\u2010performance liquid chromatography\u2010tandem mass spectrometry at 24\u2009h and 72\u2009h post\u2010ICH. The expression level of P38\u2010mitogen\u2010protein kinase (P38\u2010MAPK), myeloid differentiation factor 88 (MyD88), high\u2010mobility group box1 protein (HMGB1), and interleukin\u20101<jats:italic>\u03b2<\/jats:italic> (IL\u20101<jats:italic>\u03b2<\/jats:italic>) around hematoma was examined by western blotting at 24\u2009h. Microglial and astrocyte activation and neutrophil infiltration were examined at 72\u2009h. The lesion was examined on days 3 and 28. Neurologic deficits were examined for 28 days. A long\u2010term choline diet significantly increased serum levels of TMAO compared with a regular diet at 24\u2009h and 72\u2009h after sham operation or ICH. Choline diet\u2010induced high serum levels of TMAO did not enhance the expression of P38\u2010MAPK, MyD88, HMGB1, or IL\u20101<jats:italic>\u03b2<\/jats:italic> at 24\u2009h. However, it did increase the number of activated microglia and astrocytes around the hematoma at 72\u2009h. Contrary to our expectations, it did not aggravate acute or long\u2010term histologic damage or neurologic deficits after ICH. In summary, choline diet\u2010induced high serum levels of TMAO increased the cellular inflammatory response probably by activating microglia and astrocytes. However, it did not aggravate brain injury or worsen long\u2010term neurologic deficits. Although TMAO might be a potential risk factor for cerebrovascular diseases, this exploratory study did not support that TMAO is a promising target for ICH therapy.<\/jats:p>","DOI":"10.1155\/2022\/1599747","type":"journal-article","created":{"date-parts":[[2022,2,16]],"date-time":"2022-02-16T20:20:09Z","timestamp":1645042809000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Diet\u2010Induced High Serum Levels of Trimethylamine\u2010N\u2010oxide Enhance the Cellular Inflammatory Response without Exacerbating Acute Intracerebral Hemorrhage Injury in 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