{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T15:19:04Z","timestamp":1790695144575,"version":"4.1.0"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>JOURNAL\/nrgr\/04.03\/01300535-202407000-00033\/figure1\/v\/2026-05-11T120643Z\/r\/image-tiff<\/jats:p>\n                  <jats:p>Accumulating evidence suggests that oxidative stress and the Wnt\/\u03b2-catenin pathway participate in stroke-induced disruption of the blood-brain barrier. However, the potential links between them following ischemic stroke remain largely unknown. The present study found that cerebral ischemia leads to oxidative stress and repression of the Wnt\/\u03b2-catenin pathway. Meanwhile, Wnt\/\u03b2-catenin pathway activation by the pharmacological inhibitor, TWS119, relieved oxidative stress, increased the levels of cytochrome P450 1B1 (CYP1B1) and tight junction-associated proteins (zonula occludens-1 [ZO-1], occludin and claudin-5), as well as brain microvascular density in cerebral ischemia rats. Moreover, rat brain microvascular endothelial cells that underwent oxygen glucose deprivation\/reoxygenation displayed intense oxidative stress, suppression of the Wnt\/\u03b2-catenin pathway, aggravated cell apoptosis, downregulated CYP1B1 and tight junction protein levels, and inhibited cell proliferation and migration. Overexpression of \u03b2-catenin or knockdown of \u03b2-catenin and CYP1B1 genes in rat brain microvascular endothelial cells at least partly ameliorated or exacerbated these effects, respectively. In addition, small interfering RNA-mediated \u03b2-catenin silencing decreased CYP1B1 expression, whereas CYP1B1 knockdown did not change the levels of glycogen synthase kinase 3\u03b2, Wnt-3a, and \u03b2-catenin proteins in rat brain microvascular endothelial cells after oxygen glucose deprivation\/reoxygenation. Thus, the data suggest that CYP1B1 can be regulated by Wnt\/\u03b2-catenin signaling, and activation of the Wnt\/\u03b2-catenin\/CYP1B1 pathway contributes to alleviation of oxidative stress, increased tight junction levels, and protection of the blood-brain barrier against ischemia\/hypoxia-induced injury.<\/jats:p>","DOI":"10.4103\/1673-5374.386398","type":"journal-article","created":{"date-parts":[[2023,10,11]],"date-time":"2023-10-11T09:03:21Z","timestamp":1697015001000},"page":"1541-1547","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":39,"title":["Activation of the Wnt\/\u03b2-catenin\/CYP1B1 pathway alleviates oxidative stress and protects the blood-brain barrier under cerebral ischemia\/reperfusion conditions"],"prefix":"10.4103","volume":"19","author":[{"given":"Xingyong","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Neurology, Fujian Provincial Hospital, Shengli Clinical Medical College 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