{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,28]],"date-time":"2026-06-28T00:52:26Z","timestamp":1782607946951,"version":"3.54.5"},"reference-count":42,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2024,4,12]],"date-time":"2024-04-12T00:00:00Z","timestamp":1712880000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100002383","name":"King Saud University","doi-asserted-by":"publisher","award":["RSP2023R371"],"award-info":[{"award-number":["RSP2023R371"]}],"id":[{"id":"10.13039\/501100002383","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Ischemic stroke is a leading cause of human mortality. Cerebral ischemia\u2013reperfusion injury (CI\/RI) is a primary cause of stroke. Ischemia\u2013reperfusion (I\/R) resulting in oxidative stress and inflammatory events may lead to severe neuronal impairments. Thus, anti\u2010oxidative and anti\u2010inflammatory mediators that can alleviate post\u2010I\/R neuronal injuries are required for the treatment of CI\/RI. An alkaloid, voacangine (VCG) is a recognized antioxidant, anti\u2010inflammatory, and anticancer agent. Hence, the current study intended to explore the neuroprotective potential and the principal mechanisms of VCG in CI\/RI. The experimental rats were divided into four sets: control, I\/R\u2010induced, I\/R\u2009+\u2009VCG (2.5\u2009mg\/kg), I\/R\u2009+\u2009VCG (5\u2009mg\/kg). CI\/RI was induced by implanting a thread into the middle cerebral artery occlusion (MCAO) model. Brain damages were assessed on the basis of brain edema, brain infarct volume, neurological deficit score, histopathology, oxidative stress, and neuroinflammation. Results revealed that VCG inhibited the triggering of NLRP3 inflammasome, pro\u2010inflammatory cytokines, lipid peroxidation, but enhanced the antioxidant status in MCAO rats. Furthermore, VCG treatment averted brain damage by I\/R, neuroinflammation, and oxidative stress by suppressing NF\u2010\u03baBp65\/MAPK pathways. The results of the study provide pertinent insights pertaining to the role of VCG as a potential neuroprotective agent against ischemic stroke.<\/jats:p>","DOI":"10.1002\/tox.24274","type":"journal-article","created":{"date-parts":[[2024,4,12]],"date-time":"2024-04-12T11:33:47Z","timestamp":1712921627000},"page":"4004-4013","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Voacangine mitigates oxidative stress and neuroinflammation in <scp>middle cerebral artery occlusion<\/scp>\u2010induced cerebral ischemia\/reperfusion injury by averting the <scp>NF\u2010\u03baBp65<\/scp>\/<scp>MAPK<\/scp> signaling pathways in rats"],"prefix":"10.1002","volume":"39","author":[{"given":"Bo","family":"Xu","sequence":"first","affiliation":[{"name":"Department of General Medicine Shaanxi Provincial People's Hospital  Xi'an 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