{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T20:53:42Z","timestamp":1791665622860,"version":"4.3.4"},"reference-count":33,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2023,12,6]],"date-time":"2023-12-06T00:00:00Z","timestamp":1701820800000},"content-version":"vor","delay-in-days":5,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82001327"],"award-info":[{"award-number":["82001327"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunity Inflam &amp;amp; Disease"],"published-print":{"date-parts":[[2023,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objectives<\/jats:title><jats:p>We aimed to investigate the role of soluble epoxide hydrolase for hyperglycemia induced\u2010disruption of blood\u2010brain barrier (BBB) integrity after diffuse axonal injury (DAI).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Rat DAI hyperglycemia model was established by a lateral head rotation device and intraperitoneal injection of 50% glucose. Glial fibrillary acidic protein, ionized calcium\u2010binding adapter molecule\u20101, \u03b2\u2010amyloid precursor protein, neurofilament light chain, and neurofilament heavy chain was detected by immunohistochemistry. Cell apoptosis was examined by terminal deoxynucleotidyl transferase nick\u2010end labeling (TUNEL) assay. The permeability of blood\u2010brain barrier (BBB) was assessed by expression of tight junction proteins, leakage of Evans blue and brain water content. The soluble epoxide hydrolase (sEH) pathway was inhibited by 1\u2010trifluoromethoxyphenyl\u20103\u2010(1\u2010propionylpiperidin\u20104\u2010yl) urea (TPPU) and the nuclear transcription factor kappa B (NF\u2010\u03baB) pathway was inhibited by pyrrolidine dithiocarbamate and activated by phorbol\u201012\u2010myristate\u201013\u2010acetate in vivo and\/or vitro, respectively. The inflammatory factors were detected by enzyme\u2010linked immunosorbent assay.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Hyperglycemia could exacerbate axonal injury, aggravate cell apoptosis and glial activation, worsen the loss of BBB integrity, increase the release of inflammatory factors, and upregulate the expression of sEH and NF\u2010\u03baB. Inhibition of sEH could reverse all these damages and protect BBB integrity by upregulating the expression of tight junction proteins and downregulating the levels of inflammatory factors in vivo and vitro, while the agonist of NF\u2010\u03baB pathway abrogated the protective effects of TPPU on BBB integrity in vitro.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>sEH was involved in mediating axonal injury induced by hyperglycemia after DAI by disrupting BBB integrity through inducing inflammation via the NF\u2010\u03baB pathway.<\/jats:p><\/jats:sec>","DOI":"10.1002\/iid3.1105","type":"journal-article","created":{"date-parts":[[2023,12,6]],"date-time":"2023-12-06T12:41:10Z","timestamp":1701866470000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Hyperglycemia disrupted the integrity of the blood\u2010brain barrier following diffuse axonal injury through the sEH\/NF\u2010\u03baB 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