{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T16:26:36Z","timestamp":1767889596403,"version":"3.49.0"},"reference-count":25,"publisher":"Canadian Science Publishing","issue":"11","license":[{"start":{"date-parts":[[2015,11,1]],"date-time":"2015-11-01T00:00:00Z","timestamp":1446336000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2015,11]]},"abstract":"<jats:p> Ischemia\u2013reperfusion (I\/R) injury after a liver transplant is a major cause of severe complications that lead to graft dysfunction. Fucoidan, a complex of sulfated polysaccharides derived from marine brown algae, demonstrated antiapoptotic as well as potential anti-inflammatory properties in previous studies. Fucoidan has also shown protective effects on I\/R-injured kidney and heart. However, whether fucoidan can attenuate hepatic I\/R injury has not been examined. To clarify the role of fucoidan in hepatic I\/R injury, Sprague\u2013Dawley rats were subjected to sham operation or ischemia followed by reperfusion with treatment of saline or fucoidan (50, 100, or 200 mg\u00b7(kg body mass)<jats:sup>\u22121<\/jats:sup>\u00b7d<jats:sup>\u22121<\/jats:sup>). The fucoidan-treated group showed decreased levels of alanine aminotransferase and aspartate aminotransferase compared with the control group. Myeloperoxidase and malondialdehyde activities and mRNA levels of CD11b in the fucoidan-treated group were significantly decreased. Hepatocellular swelling\/necrosis, sinusoidal\/vascular congestion, and inflammatory cell infiltration were also attenuated in the fucoidan group. The expression of TNF-\u03b1, IL-6, IL-1\u03b2, CXCL-10, VCAM-1, and ICAM-1 were markedly decreased in the samples from the fucoidan-treated group. Fucoidan largely prevented activation of the inflammatory signaling pathway, compared with the control group. In summary, fucoidan can protect the liver from I\/R injury through suppressing activation of the inflammatory signaling pathway, as well as the expression of inflammatory mediators, and inflammatory cell infiltration. <\/jats:p>","DOI":"10.1139\/cjpp-2015-0120","type":"journal-article","created":{"date-parts":[[2015,6,1]],"date-time":"2015-06-01T21:15:58Z","timestamp":1433193358000},"page":"999-1005","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":33,"title":["Fucoidan reduces inflammatory response in a rat model of hepatic ischemia\u2013reperfusion injury"],"prefix":"10.1139","volume":"93","author":[{"given":"Xiao-jing","family":"Li","sequence":"first","affiliation":[{"name":"Transplant Medical Engineering Research Center, Third Xiangya Hospital, Central South University, Hunan, China."},{"name":"Transplant Medical Engineering Research Center, Third Xiangya Hospital, Central South University, Hunan, China."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qi-fa","family":"Ye","sequence":"additional","affiliation":[{"name":"Transplant Medical Engineering Research Center, Third Xiangya Hospital, Central South University, Hunan, China."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-6143.2006.01595.x"},{"key":"refg2\/ref2","doi-asserted-by":"publisher","DOI":"10.1017\/S0007114508137886"},{"key":"refg3\/ref3","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6215(02)00053-8"},{"key":"refg4\/ref4","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0056224"},{"key":"refg5\/ref5","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6215(99)00148-2"},{"key":"refg6\/ref6","doi-asserted-by":"publisher","DOI":"10.1093\/glycob\/cwm014"},{"key":"refg7\/ref7","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-4800(03)00008-X"},{"key":"refg8\/ref8","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.00568.2005"},{"key":"refg9\/ref9","doi-asserted-by":"publisher","DOI":"10.1172\/JCI12568"},{"key":"refg10\/ref10","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e3182308c64"},{"key":"refg11\/ref11","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199712000-00003"},{"key":"refg12\/ref12","doi-asserted-by":"publisher","DOI":"10.1189\/jlb.0307180"},{"key":"refg13\/ref13","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2013.5486"},{"key":"refg14\/ref14","doi-asserted-by":"publisher","DOI":"10.1160\/TH05-08-0546"},{"key":"refg15\/ref15","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9610(00)00573-0"},{"issue":"1","key":"refg16\/ref16","first-page":"1","volume":"16","author":"Su J.F.","year":"2003","journal-title":"Biomed. 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