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The goal of this study was to explore if post\u2010stroke exercise conditioning (PostE) reduced brain injury and whether it was associated with the regulation of gluconeogenesis. Adult rats received 2\u00a0h of middle cerebral artery (MCA) occlusion, followed by 24\u00a0h of reperfusion. Treadmill activity was then initiated 24\u00a0h after reperfusion for PostE. The severity of the brain damage was determined by infarct volume, apoptotic cell death, and neurological deficit at one and three days after reperfusion. We measured gluconeogenesis including oxaloacetate (OAA), phosphoenolpyruvate (PEP), pyruvic acid, lactate, ROS, and glucose via ELISA, as well as the location and expression of the key enzyme phosphoenolpyruvate carboxykinase (PCK)\u20101\/2 via immunofluorescence. We also determined upstream pathways including forkhead transcription factor (FoxO1), p\u2010FoxO1, 3\u2010kinase (PI3K)\/Akt, and p\u2010PI3K\/Akt via Western blot. Additionally, the cytoplasmic expression of p\u2010FoxO1 was detected by immunofluorescence. Compared to non\u2010exercise control, PostE (*\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a0.05) decreased brain infarct volumes, neurological deficits, and cell death at one and three days. PostE groups (*\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a0.05) saw increases in OAA and decreases in PEP, pyruvic acid, lactate, ROS, glucose levels, and tissue PCKs expression on both days. PCK\u20101\/2 expressions were also significantly (*\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a0.05) suppressed by the exercise setting. Additionally, phosphorylated PI3K, AKT, and FoxO1 protein expression were significantly induced by PostE at one and three days (*\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a0.05). In this study, PostE reduced brain injury after stroke, in association with activated PI3K\/AKT\/FoxO1 signaling, and inhibited gluconeogenesis. These results suggest the involvement of FoxO1 regulation of gluconeogenesis underlying post\u2010stroke neuroprotection.\n                  <\/jats:p>","DOI":"10.1002\/brb3.2805","type":"journal-article","created":{"date-parts":[[2022,11,30]],"date-time":"2022-11-30T03:10:50Z","timestamp":1669777850000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Exercise postconditioning reduces ischemic injury via suppression of cerebral gluconeogenesis in rats"],"prefix":"10.1002","volume":"13","author":[{"given":"Fengwu","family":"Li","sequence":"first","affiliation":[{"name":"China\u2010America Institute of Neuroscience Beijing Luhe Hospital, Capital Medical University  Beijing China"},{"name":"Department of Developmental Cell Biology Key Laboratory of Cell Biology, Ministry of Public Health, and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University  Shenyang 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