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Protective effects of trehalose preconditioning on cardiac and coronary endothelial function through eNOS signaling pathway in a rat model of ischemia-reperfusion injury
| Title: | Protective effects of trehalose preconditioning on cardiac and coronary endothelial function through eNOS signaling pathway in a rat model of ischemia-reperfusion injury |
| Authors: | Suno, Kenichiro Browse this author | | Shingu, Yasushige Browse this author →KAKEN DB | | Wakasa, Satoru Browse this author →KAKEN DB |
| Keywords: | Trehalose | | Endothelial dysfunction | | Endothelial nitric oxide synthase | | Ischemia-reperfusion injury | | Cardioprotection |
| Issue Date: | 1-Oct-2023 |
| Publisher: | Springer |
| Journal Title: | Molecular and cellular biochemistry |
| Volume: | 477 |
| Issue: | 10 |
| Start Page: | 2403 |
| End Page: | 2414 |
| Publisher DOI: | 10.1007/s11010-022-04451-y |
| Abstract: | Coronary endothelial dysfunction is a major cause of ischemia-reperfusion (I/R) injury. Trehalose, a natural disaccharide, has been reported to ameliorate endothelial dysfunction during aging by activating endothelial nitric oxide synthase (eNOS); however, its role in I/R injury is unknown. This study evaluated the effects of trehalose preconditioning on cardiac and coronary endothelial function after I/R. Langendorff-perfused rat hearts underwent 30 min of global ischemia followed by 80 min of reperfusion with or without trehalose preconditioning. Rate pressure product (RPP) and coronary flow (CF) were measured during reperfusion. Perivascular edema was assessed by hematoxylin and eosin staining. Myocardial oxidative stress and apoptosis were evaluated by immunohistochemistry and TUNEL staining, respectively. eNOS dimerization was determined by western blotting. An eNOS inhibitor was used to examine the role of eNOS. Trehalose preconditioning showed a higher recovery rate after I/R as indicated by high RPP (control vs. trehalose, 28 +/- 6% vs. 46 +/- 9%; P = 0.017, Cohen's d = 2.3) and CF values (35 +/- 10% vs. 55 +/- 9%; P = 0.025, d = 1.7). Furthermore, trehalose preconditioning reduced perivascular edema, myocardial oxidative stress, and apoptosis. The eNOS dimerization ratio was increased by trehalose (1.2 +/- 0.2 vs. 1.6 +/- 0.2; P = 0.023, d = 2.1), which was associated with the recovery of RPP and CF. These effects of trehalose were abolished by the eNOS inhibitor. Trehalose preconditioning showed protective effects on cardiac and coronary endothelial function after I/R through the eNOS signaling pathway. |
| Rights: | This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: http://dx.doi.org/10.1007/s11010-022-04451-y |
| Type: | article (author version) |
| URI: | http://hdl.handle.net/2115/90587 |
| Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 新宮 康栄
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