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Autor(en) / Beteiligte
Titel
Oleanolic acid attenuates liver ischemia reper-fusion injury by HO-1/Sesn2 signaling pathway
Ist Teil von
  • 国际肝胆胰疾病杂志(英文版), 2016, Vol.15 (5), p.519-524
Ort / Verlag
Department of Liver Surgery, First Afifliated Hospi-tal of Nanjing Medical University, Key Laboratory of Living Donor Liver Transplantation of Ministry of Public Health, Nanjing 210029, China
Erscheinungsjahr
2016
Link zum Volltext
Quelle
Elsevier ScienceDirect Journals
Beschreibungen/Notizen
  • BACKGROUND: Ischemia reperfusion injury (IRI) is unavoid-able in liver transplantation and hepatectomy. The present study aimed to explore the possible mechanism and the effect of oleanolic acid (OA) in hepatic IRI. METHODS: Mice were randomly divided into 6 groups based on different treatment. IRI model: The hepatic artery, portal vein, and bile duct to the left and median liver lobes (70% of the liver) were occluded with an atraumatic bulldog clamp for 90 minutes and then the clamp was removed for reperfusion. The mice were sacriifced 6 hours after reperfusion, and blood and liver tissues were collected. Liver injury was evaluated by biochemical and histopathologic examinations. The expressions of Sesn2, PI3K, Akt and heme oxygenase-1 (HO-1) were mea-sured with quantitative real-time RT-PCR and Western blotting. RESULTS: The serum aminotransferases level and scores of he-patic histology were increased after reperfusion. The increase was attenuated by pretreatment with OA (P<0.01). Compared with the IR group, OA pretreatment signiifcantly up-regulated the expression of Sesn2, PI3K, Akt and HO-1 in IR livers (P<0.05). Administration of zinc protoporphyrin (ZnPP), an inhibitor of HO-1, diminished the OA effect on HO-1 and Sesn2 expressions (P<0.05) and the protective effect of OA on IRI. CONCLUSIONS: Our results demonstrate that OA can attenu-ate hepatic IRI. The protective mechanism may be related to the OA-induced HO-1/Sesn2 signaling pathway.
Sprache
Englisch
Identifikatoren
ISSN: 1499-3872
DOI: 10.1016/S1499-3872(16)60115-7
Titel-ID: cdi_wanfang_journals_gjgdybzz_z201605012
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