{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T20:53:32Z","timestamp":1788382412728,"version":"build-2803163510"},"reference-count":47,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2024,2,23]],"date-time":"2024-02-23T00:00:00Z","timestamp":1708646400000},"content-version":"vor","delay-in-days":22,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Chem Biol Drug Des"],"published-print":{"date-parts":[[2024,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Neuroinflammation contributes to neurological dysfunction in the patients who suffer from subarachnoid hemorrhage (SAH). Isoliquiritigenin (ISL) is a bioactive component extracted from <jats:italic>Genus Glycyrrhiza<\/jats:italic>. This work is to investigate whether ISL ameliorates neuroinflammation after SAH. In this study, intravascular perforation of male Sprague\u2013Dawley rats was used to establish a SAH model. ISL was administered by intraperitoneal injection 6\u2009h after SAH in rats. The mortality, SAH grade, neurological score, brain water content, and blood\u2013brain barrier (BBB) permeability were examined at 24\u2009h after the treatment. Expressions of tumor necrosis factor\u2010\u03b1, interleukin\u20106, Iba\u20101, and MPO were measured by quantitative real\u2010time polymerase chain reaction (qRT\u2010PCR). Besides, the expression levels of NF\u2010\u03baB p65 and NLRP3, ASC, caspase\u20101, IL\u20101\u03b2, and IL\u201018 were analyzed by western blot. The experimental data suggested that ISL treatment could ameliorate neurological impairment, attenuate brain edema, and ameliorate BBB injury after SAH in rats. ISL treatment repressed the expression of proinflammatory cytokines TNF\u2010\u03b1 and IL\u20106, and meanwhile inhibited the expression of Iba\u20101 and MPO. ISL also repressed NF\u2010\u03baB p65 expression as well as the transport from the cytoplasm to the nucleus. In addition, ISL significantly suppressed the expression levels of NLR family pyrin domain containing 3 (NLRP3), ASC, caspase\u20101, IL\u20101\u03b2, and IL\u201018. These findings suggest that ISL inactivates NLRP3 pathway by inhibiting NF\u2010\u03baB p65 translocation, thereby repressing the neuroinflammation after SAH, and it is a potential drug for the treatment of SAH.<\/jats:p>","DOI":"10.1111\/cbdd.14436","type":"journal-article","created":{"date-parts":[[2024,2,24]],"date-time":"2024-02-24T02:04:38Z","timestamp":1708740278000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Isoliquiritigenin attenuates neuroinflammation after subarachnoid hemorrhage through inhibition of <scp>NF\u2010\u03baB<\/scp>\u2010mediated <scp>NLRP3<\/scp> inflammasome activation"],"prefix":"10.1111","volume":"103","author":[{"given":"Zhang","family":"Wenfei","sequence":"first","affiliation":[{"name":"Department of Neurosurgery Renmin Hospital of Wuhan University  Wuhan 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