{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,28]],"date-time":"2026-06-28T10:49:19Z","timestamp":1782643759125,"version":"3.54.5"},"reference-count":58,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2020,4,17]],"date-time":"2020-04-17T00:00:00Z","timestamp":1587081600000},"content-version":"vor","delay-in-days":107,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100007620","name":"Department of Education of Liaoning Province","doi-asserted-by":"publisher","award":["LK201651"],"award-info":[{"award-number":["LK201651"]}],"id":[{"id":"10.13039\/501100007620","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Immunology Research"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:p>\n                    Acute kidney injury (AKI) is one of the most common and troublesome perioperative complications. Dexmedetomidine (DEX) is a potent\n                    <jats:italic>\u03b1<\/jats:italic>\n                    2\u2010adrenoceptor (\n                    <jats:italic>\u03b1<\/jats:italic>\n                    2\u2010AR) agonist with anti\u2010inflammatory and renoprotective effects. In this study, a rat renal ischemia\u2013reperfusion injury (IRI) model was induced. At 24\u2009h after reperfusion, the IRI\u2010induced damage and the renoprotection of DEX preconditioning were confirmed both biochemically and histologically. Changes in nuclear factor\u2010kappa B (NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B), as well as its downstream anti\u2010inflammatory factor A20 and proinflammatory factor tumor necrosis factor\u2010\n                    <jats:italic>\u03b1<\/jats:italic>\n                    (TNF\u2010\n                    <jats:italic>\u03b1<\/jats:italic>\n                    ), were detected. Atipamezole, a nonselective antagonist, was then added 5\u2009min before the administration of DEX to further analyze DEX\u2019s effects on NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B, and another anti\u2010inflammatory medicine, methylprednisolone, was used in comparison with DEX, to further analyze DEX\u2019s effects on NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B. Different concentrations of DEX (0\u2009nM, 0.1\u2009nM, 1\u2009nM, 10\u2009nM, 100\u2009nM, 1\u2009\n                    <jats:italic>\u03bc<\/jats:italic>\n                    M, and 10\u2009\n                    <jats:italic>\u03bc<\/jats:italic>\n                    M) were applied to preincubated human renal tubular epithelial cell line (HK\u20102) cells in vitro. After anoxia and reoxygenation, the MTT (3\u2010(4,5\u2010dimethylthiazol\u20102\u2010yl)\u20102,5\u2010diphenyltetrazolium bromide) tetrazolium assay and enzyme\u2010linked immunosorbent assay (ELISA) were performed to evaluate the levels of NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B downstream anti\u2010inflammatory cytokines. The results showed that, unlike methylprednisolone, DEX preconditioning led to a time\u2010dependent biphasic change (first activation then inhibition) of NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B in the rat renal IRI models that were given 25\u2009\n                    <jats:italic>\u03bc<\/jats:italic>\n                    g\/kg i.p. It was accompanied by a similarly biphasic change of TNF\u2010\n                    <jats:italic>\u03b1<\/jats:italic>\n                    and an early and persistent upregulation of A20. In vitro, DEX\u2019s cellular protection showed a concentration\u2010dependent biphasic change which was protective within the range of 0 to 100\u2009nM but became opposite when concentrations are greater than 1\u2009\n                    <jats:italic>\u03bc<\/jats:italic>\n                    M. The changes in the A20 and NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B messenger RNA (mRNA) levels were consistent with the renoprotective ability of DEX. In other words, DEX preconditioning protected the rats from renal IRI via regulation biphasic change of NF\u2010\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B signaling.\n                  <\/jats:p>","DOI":"10.1155\/2020\/3230490","type":"journal-article","created":{"date-parts":[[2020,4,17]],"date-time":"2020-04-17T19:30:37Z","timestamp":1587151837000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Dexmedetomidine Preconditioning Protects Rats from Renal Ischemia\u2013Reperfusion Injury Accompanied with Biphasic Changes of Nuclear Factor\u2010Kappa B 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