{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T04:49:34Z","timestamp":1777870174071,"version":"3.51.4"},"reference-count":43,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,10,18]],"date-time":"2019-10-18T00:00:00Z","timestamp":1571356800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Dexmedetomidine (Dex) has been proven to exert protective effects on multiple organs in response to ischaemia\u2010reperfusion injury, but the specific mechanism by which this occurs has not been fully elucidated. The purpose of this study was to investigate whether Dex attenuates spinal cord ischaemia\u2010reperfusion injury (SCIRI) by inhibiting endoplasmic reticulum stress (ERS). Our team established a model of SCIRI and utilized the endoplasmic reticulum agonist thapsigargin. Dex (25\u00a0g\/kg) was intraperitoneally injected 30\u00a0minutes before spinal cord ischaemia. After 45\u00a0minutes of ischaemia, the spinal cord was reperfused for 24\u00a0hours. To evaluate the neuroprotective effect of Dex on SCIRI, neurological function scores were assessed in rats and apoptosis of spinal cord cells was determined by TUNEL staining. To determine whether the endoplasmic reticulum apoptosis pathway CNPY2\u2010PERK was involved in the neuroprotective mechanism of Dex, the expression levels of related proteins (CNPY2, GRP78, PERK, CHOP, caspase\u201012, caspase\u20109 and caspase\u20103) were detected by western blot analysis and RT\u2010PCR. We observed that Dex significantly increased the neurological function scores after SCIRI and decreased apoptosis of spinal cord cells. The expression of ERS\u2010related apoptosis proteins was significantly increased by SCIRI but was significantly decreased in response to Dex administration. Taken together, the results of this study indicate that Dex may attenuate SCIRI by inhibiting the CNPY2\u2010ERS apoptotic pathway.<\/jats:p>","DOI":"10.1111\/jcmm.14688","type":"journal-article","created":{"date-parts":[[2019,10,18]],"date-time":"2019-10-18T09:42:35Z","timestamp":1571391755000},"page":"8173-8183","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Dexmedetomidine attenuates neuronal injury after spinal cord ischaemia\u2010reperfusion injury by targeting the CNPY2\u2010endoplasmic reticulum stress signalling"],"prefix":"10.1111","volume":"23","author":[{"given":"Lina","family":"Zhao","sequence":"first","affiliation":[{"name":"Department of Anaesthesiology Tianjin Hospital Tianjin China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Meili","family":"Zhai","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology Tianjin Central Hospital of Gynecology Obstetrics 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