{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,8]],"date-time":"2026-02-08T03:45:51Z","timestamp":1770522351669,"version":"3.49.0"},"reference-count":60,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[2001,10]]},"abstract":"<jats:p><jats:bold><jats:italic><jats:bold><jats:italic>Background and Purpose<\/jats:italic><\/jats:bold>\u2014<\/jats:italic><\/jats:bold>Nuclear factor-\u03baB (NF-\u03baB) and the signal transducer and activator of transcription 3 (STAT3) are important transcription factors regulating inflammatory mechanisms and the glial response to neural injury, determining lesion outcome. In this study we evaluate the ability of triflusal (2-acetoxy-4-trifluoromethylbenzoic acid), an antiplatelet agent inhibitor of NF-\u03baB activation, to improve lesion outcome after excitotoxic damage to the immature brain.<\/jats:p><jats:p><jats:bold><jats:italic><jats:bold><jats:italic>Methods<\/jats:italic><\/jats:bold>\u2014<\/jats:italic><\/jats:bold>Postnatal day 9 rats received an intracortical injection of the excitotoxin<jats:italic>N<\/jats:italic>-methyl-<jats:sc>d<\/jats:sc>-aspartate (NMDA) and oral administration of triflusal (30 mg\/kg) either as 3 doses before NMDA injection (pretreatment) or as a single dose 8 hours after NMDA injection (posttreatment). After survival times of 10 and 24 hours, brains were processed for toluidine blue staining, tomato lectin histochemistry, and glial fibrillary acidic protein, NF-\u03baB, and STAT3 immunocytochemistry.<\/jats:p><jats:p><jats:bold><jats:italic><jats:bold><jats:italic>Results<\/jats:italic><\/jats:bold>\u2014<\/jats:italic><\/jats:bold>NMDA-lesioned animals that were not treated with triflusal showed activation of NF-\u03baB in neuronal cells at first and in glial cells subsequently. Animals that received pretreatment with triflusal showed a strong downregulation of neuronal and glial NF-\u03baB but a similar development of the glial response and an equivalent lesion volume compared with nontreated animals. In contrast, animals receiving triflusal posttreatment showed increased early neuronal NF-\u03baB but a reduction in the subsequent glial NF-\u03baB, accompanied by important downregulation of the microglial and astroglial response and a drastic reduction in the lesion size. STAT3 activation was not affected by triflusal treatment.<\/jats:p><jats:p><jats:bold><jats:italic><jats:bold><jats:italic>Conclusions<\/jats:italic><\/jats:bold>\u2014<\/jats:italic><\/jats:bold>Triflusal posttreatment diminishes glial NF-\u03baB, downregulates the glial response, and improves the lesion outcome, suggesting a neuroprotective role of this compound against excitotoxic injury in the immature brain.<\/jats:p>","DOI":"10.1161\/hs1001.097243","type":"journal-article","created":{"date-parts":[[2007,10,10]],"date-time":"2007-10-10T17:46:58Z","timestamp":1192038418000},"page":"2394-2402","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":36,"title":["Triflusal Posttreatment Inhibits Glial Nuclear Factor-\u03baB, Downregulates the Glial Response, and Is Neuroprotective in an Excitotoxic Injury Model in Postnatal Brain"],"prefix":"10.1161","volume":"32","author":[{"given":"Laia","family":"Acarin","sequence":"first","affiliation":[{"name":"From the Unit of Histology, School of Medicine, Department of Cell Biology, Physiology, and Immunology, Autonomous University of Barcelona, Bellaterra, Spain."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Berta","family":"Gonza\u0301lez","sequence":"additional","affiliation":[{"name":"From the Unit of Histology, School of Medicine, Department of Cell Biology, Physiology, and Immunology, Autonomous University of Barcelona, Bellaterra, Spain."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bernardo","family":"Castellano","sequence":"additional","affiliation":[{"name":"From the Unit of Histology, School of Medicine, Department of Cell Biology, Physiology, and Immunology, Autonomous University of Barcelona, Bellaterra, Spain."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(96)01073-6"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0169-328X(98)00330-1"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1097\/00001756-199808240-00035"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/jnen\/59.2.151"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1136(199604)16:4<306::AID-GLIA3>3.0.CO;2-Y"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(95)11919-N"},{"key":"e_1_3_2_7_2","first-page":"159","volume":"735","year":"1996","unstructured":"Terai K, Matsuo A, McGeer PL. 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