{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T22:08:16Z","timestamp":1787004496143,"version":"build-2736575974"},"reference-count":39,"publisher":"Portland Press Ltd.","issue":"5","license":[{"start":{"date-parts":[[2019,7,25]],"date-time":"2019-07-25T00:00:00Z","timestamp":1564012800000},"content-version":"vor","delay-in-days":281,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2018,10,31]]},"abstract":"<jats:p>The present study was designed to determine whether glycogen synthase kinase-3\u03b2 (GSK-3\u03b2) was involved in the cardioprotection by \u03b17 nicotinic acetylcholine receptor (\u03b17nAChR) agonist and limb remote ischemic postconditionings. Forty male Sprague-Dawley rats were randomly divided equally into control (C), \u03b17nAChR agonist postconditioning (P), limb remote ischemic postconditioning (L), combined \u03b17nAChR agonist and limb remote ischemic postconditioning (P+L) groups. At the end of experiment, serum cTnI, creatine kinase-MB (CK-MB), tumor necrosis factor-\u03b1 (TNF-\u03b1), interleukin-6 (IL-6), high mobility group protein (HMGB1) and interleukin-10 (IL-10) levels were measured; infarct size (IS), myocardial expressions of GSK-3\u03b2, p-GSK-3\u03b2 (Ser9), nuclear factor-\u03baB (NF-\u03baB) and p-NF-\u03baB (Ser536) in the ischemic area were assessed. The results showed that compared with group C, IS, serum cTnI and CK-MB levels obviously decreased in groups P, L and P+L. Compared with groups P and L, IS, serum cTnI and CK-MB levels significantly decreased in group P+L. Compared with group C, serum TNF-\u03b1, IL-6 and HMGB1 levels, and myocardial expression of p-NF-\u03baBp65 (Ser536) evidently decreased, and myocardial expression of p-GSK-3\u03b2 (Ser9) obviously increased in groups P, L and P+L. Compared with group P, serum TNF-\u03b1, IL-6 and HMGB1 levels and myocardial expression of p-NF-\u03baBp65 (Ser536) significantly increased, and myocardial expression of p-GSK-3\u03b2 (Ser9) evidently decreased in group L. Compared with group L, serum TNF-\u03b1, IL-6, HMGB1 levels, and myocardial expression of p-NF-\u03baBp65 (Ser536) significantly decreased, and myocardial expression of p-GSK-3\u03b2 (Ser9) obviously increased in group P+L. In conclusion, our findings indicate that inhibition of GSK-3\u03b2 to decrease NF-\u03baB transcription is one of cardioprotective mechanisms of \u03b17nAChR agonist and limb remote ischemic postconditionings by anti-inflammation, but improved cardioprotection by combined two interventions is not completely attributable to an enhanced anti-inflammatory mechanism.<\/jats:p>","DOI":"10.1042\/bsr20181315","type":"journal-article","created":{"date-parts":[[2018,9,24]],"date-time":"2018-09-24T12:15:27Z","timestamp":1537791327000},"update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Inhibition of glycogen synthase kinase-3\u03b2 is involved in cardioprotection by \u03b17nAChR agonist and limb remote ischemic postconditionings"],"prefix":"10.1042","volume":"38","author":[{"given":"Hui-Xian","family":"Li","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin-Long","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1028-6036","authenticated-orcid":false,"given":"Fu-Shan","family":"Xue","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gui-Zhen","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ya-Yang","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xu","family":"Liao","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2018,10,17]]},"reference":[{"key":"2021111619132578100_B1","doi-asserted-by":"publisher","first-page":"46","DOI":"10.7150\/ijbs.16404","article-title":"The protective effect of \u03b17 nicotinic acetylcholine receptor activation on critical illness and its mechanism","volume":"13","author":"Ren","year":"2017","journal-title":"Int J. 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