{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T23:08:48Z","timestamp":1789168128447,"version":"build-2803163510"},"reference-count":52,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2024,9,18]],"date-time":"2024-09-18T00:00:00Z","timestamp":1726617600000},"content-version":"vor","delay-in-days":17,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Brain and Behavior"],"published-print":{"date-parts":[[2024,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Hypoxia inducible factor\u20101\u03b1 (HIF\u20101\u03b1) is a sensitive indicator of oxygen homeostasis, of which the expression elevates following hypoxia\/ischemia. This study reveals the specific mechanisms underlying the effects of HIF\u20101\u03b1 on ischemic stroke (IS).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>IS model was established using middle cerebral artery occlusion (MCAO)\u2010modeled male rats and oxygen glucose deprivation\/reoxygenation (OGD\/R)\u2010treated mice hippocampal cells HT22, followed by the silencing of HIF\u20101\u03b1 and the overexpression of C\u2010X\u2010C motif chemokine receptor 4 (CXCR4) and nuclear factor\u2010kappa B (NF\u2010\u03baB). Following the surgery, Garcia's grading scale was applied for neurological evaluation. Cerebral infarcts and injuries were visualized using 2,3,5\u2010triphenyltetrazolium chloride and hematoxylin\u2010eosin staining. The levels of tumor necrosis factor\u2010\u03b1, Interleukin (IL)\u20106, IL\u20101\u03b2, malondialdehyde, and 8\u2010hydroxy\u20102\u2032\u2010deoxyguanosine, were calculated via ELISA. MTT assay and lactate dehydrogenase (LDH) assay kit were adopted to determine the viability and cytotoxicity of OGD\/R\u2010modeled cells. Reactive oxygen species (ROS) generation was evaluated using a 2\u2032\u20107\u2032dichlorofluorescin diacetate (DCFH\u2010DA) probe. The levels of HIF\u20101\u03b1, CXCR4, and NF\u2010\u03baB p65 were quantified via Western blot and immunofluorescence, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>HIF\u20101\u03b1 knockdown improved Garcia's score, attenuated the cerebral infarct, inflammation, and ROS generation, and alleviated the levels of inflammatory cytokines and CXCR4\/NF\u2010\u03baB p65 in MCAO\u2010modeled rats. Such effects were reversed following the overexpression of CXCR4 and NF\u2010\u03baB. Also, in OGD\/R\u2010treated HT22 cells, HIF\u20101\u03b1 silencing diminished the cytotoxicity and ROS production and reduced the expressions of CXCR4\/NF\u2010\u03baB p65, while promoting viability. However, CXCR4\/NF\u2010\u03baB p65 overexpression did the opposite.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>HIF\u20101\u03b1 knockdown alleviates inflammation and oxidative stress in IS through the CXCR4\/NF\u2010\u03baB pathway.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/brb3.70039","type":"journal-article","created":{"date-parts":[[2024,9,19]],"date-time":"2024-09-19T01:04:55Z","timestamp":1726707895000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["HIF\u20101\u03b1 knockdown attenuates inflammation and oxidative stress in ischemic stroke male rats via CXCR4\/NF\u2010\u03baB pathway"],"prefix":"10.1002","volume":"14","author":[{"given":"Gao","family":"Chen","sequence":"first","affiliation":[{"name":"School of Medicine Quzhou College of Technology Quzhou Zhejiang 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