{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T20:47:45Z","timestamp":1793479665722,"version":"4.5.0"},"reference-count":40,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,7,7]],"date-time":"2022-07-07T00:00:00Z","timestamp":1657152000000},"content-version":"vor","delay-in-days":187,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81971805"],"award-info":[{"award-number":["81971805"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:p>Ketone bodies including <jats:italic>\u03b2<\/jats:italic>\u2010hydroxybutyrate (<jats:italic>\u03b2<\/jats:italic>\u2010HB) have been proved the therapeutic potential in diverse neurological disorders. However, the role of <jats:italic>\u03b2<\/jats:italic>\u2010HB in the regulation of neurological injury after cardiac arrest (CA) remains unclear. We investigated the effect of <jats:italic>\u03b2<\/jats:italic>\u2010HB on brain mitochondrial dysfunction and neurological function after CA. A rat model of CA was established by asphyxia. The rats were randomly divided into three groups: sham group, control group, and <jats:italic>\u03b2<\/jats:italic>\u2010HB group. Animals received 200\u2009mg\/kg <jats:italic>\u03b2<\/jats:italic>\u2010HB or same volume vehicle at 10 minutes after return of spontaneous circulation by intraperitoneal injection. Neurological function was evaluated by neurologic deficit score and Y\u2010maze. Neuronal cell loss and apoptosis were detected through hematoxylin\u2010eosin staining, Nissl staining, and TdT\u2010mediated dUTP nick\u2010end labeling assay. Oxidative stress levels were determined by immunohistochemical staining of 4\u2010hydoxynonenal and 8\u2010hydroxy\u20102\u2009<jats:sup>\u2032<\/jats:sup>\u2010deoxyguanosine. Furthermore, mitochondrial ultrastructure of brain cells was observed by transmission electron microscopy. In addition, the protein expression levels of Bak, caspase 3, gasdermin D, caspase 1, brain\u2010derived neurotrophic factor, dynamin\u2010related protein 1 (Drp1), and phospho\u2010Drp1 (ser616) were measured. We found that neurological function and survival rate were significantly higher in the <jats:italic>\u03b2<\/jats:italic>\u2010HB group compared with the control group. <jats:italic>\u03b2<\/jats:italic>\u2010HB also reduced neurons death and neurological oxidative stress after CA. Moreover, <jats:italic>\u03b2<\/jats:italic>\u2010HB reduced neurological injury from apoptosis and pyroptosis after CA. In addition, <jats:italic>\u03b2<\/jats:italic>\u2010HB maintained the structural integrity of brain mitochondria, prevented mitochondrial fission, and increased brain energy metabolism after CA. In conclusion, <jats:italic>\u03b2<\/jats:italic>\u2010HB beneficially affected the neurological function of rats after global cerebral ischemia, associated with decreased mitochondrial fission, and improved mitochondrial function. Our results suggest that <jats:italic>\u03b2<\/jats:italic>\u2010HB might benefit patients suffering from neurological dysfunction after CA.<\/jats:p>","DOI":"10.1155\/2022\/7736416","type":"journal-article","created":{"date-parts":[[2022,7,8]],"date-time":"2022-07-08T03:35:05Z","timestamp":1657251305000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Ketone Body Improves Neurological Outcomes after Cardiac Arrest by Inhibiting Mitochondrial Fission in 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