{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:50:37Z","timestamp":1787017837017,"version":"build-2736575974"},"reference-count":48,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,11,9]],"date-time":"2021-11-09T00:00:00Z","timestamp":1636416000000},"content-version":"vor","delay-in-days":312,"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":["82060228"],"award-info":[{"award-number":["82060228"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004001","name":"Guizhou Provincial Science and Technology Department","doi-asserted-by":"publisher","award":["QiankeheZhicheng [2021] normal 077"],"award-info":[{"award-number":["QiankeheZhicheng [2021] normal 077"]}],"id":[{"id":"10.13039\/501100004001","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":[[2021,1]]},"abstract":"<jats:p>\n                    Subarachnoid hemorrhage (SAH) is a cerebrovascular disease associated with high morbidity and mortality. CXCR4 provides neuroprotective effects, which can alleviate brain injury and inflammation induced by stroke. Previous studies have suggested that CXCR4 reduces the pyroptosis of LPS\u2010stimulated BV2 cells. The purpose of this study was to evaluate the antipyroptosis effects and mechanisms of CXCR4 after SAH. SAH animal model was induced via endovascular perforation. A total of 136 male Sprague\u2010Dawley rats were used. Recombinant human cysteine\u2010X\u2010cysteine chemokine ligand 12 (rh\u2010CXCL\u201012) was administered intranasally at 1\u2009h after SAH induction. To investigate the underlying mechanism, the inhibitor of CXCR4, AMD3100, was administered intraperitoneally at 1\u2009h before SAH. The neurobehavior tests were assessed, followed by performing Western blot and immunofluorescence staining. The Western blot results suggested that the expressions of endogenous CXCL\u201012, CXCR4, and NLRP1 were increased and peaked at 24\u2009h following SAH. Immunofluorescence staining showed that CXCR4 was expressed on neurons, microglia, and astrocytes. Rh\u2010CXCL\u201012 treatment improved the neurological deficits and reduced the number of FJC\u2010positive cells, IL\u201018\u2010positive neurons, and cleaved caspase\u20101(CC\u20101)\u2010positive neurons after SAH. Meanwhile, rh\u2010CXCL\u201012 treatment increased the levels of CXCL\u201012 and CXCR4, and reduced the levels of NLRP1, IL\u201018, IL\u20101\n                    <jats:italic>\u03b2<\/jats:italic>\n                    , and CC\u20101. Moreover, the administration of AMD3100 abolished antipyroptosis effects of CXCL\u201012 and its regulation of CXCR4 post\u2010SAH. The CXCR4\/NLRP1 signaling pathway may be involved in CXCL\u201012\u2010mediated neuronal pyroptosis after SAH. Early administration of CXCL\u201012 may be a preventive and therapeutic strategy against brain injury after SAH.\n                  <\/jats:p>","DOI":"10.1155\/2021\/6966394","type":"journal-article","created":{"date-parts":[[2021,11,9]],"date-time":"2021-11-09T14:35:30Z","timestamp":1636468530000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Rh\u2010CXCL\u201012 Attenuates Neuronal Pyroptosis after Subarachnoid Hemorrhage in Rats via Regulating the CXCR4\/NLRP1 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