Full metadata record
DC Field | Value | Language |
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dc.contributor.author | Junji Yodoi | - |
dc.date.accessioned | 2016-08-28T11:08:01Z | - |
dc.date.available | 2016-08-28T11:08:01Z | - |
dc.date.issued | 2013 | - |
dc.identifier.issn | 0090-3493 | - |
dc.identifier.other | OAK-13909 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/229851 | - |
dc.description.abstract | OBJECTIVES:: Influenza virus infections can cause severe acute lung injury leading to significant morbidity and mortality. Thioredoxin-1 is a redox-active defensive protein induced in response to stress conditions. Animal experiments have revealed that thioredoxin-1 has protective effects against various severe disorders. This study was undertaken to evaluate the protective effects of recombinant human thioredoxin-1 administration on influenza A virus (H1N1)-induced acute lung injury in mice. DESIGN:: Prospective animal trial. SETTING:: Research laboratory. SUBJECTS:: Nine-week-old male C57BL/6 mice inoculated with H1N1. INTERVENTION:: The mice were divided into a vehicle-treated group and recombinant human thioredoxin-1-treated group. For survival rate analysis, the vehicle or recombinant human thioredoxin-1 was administered intraperitoneally every second day from day-1 to day 13. For lung lavage and pathological analyses, vehicle or recombinant human thioredoxin-1 was administered intraperitoneally on days-1, 1, and 3. MEASUREMENTS AND MAIN RESULTS:: Lung lavage and pathological analyses were performed at 24, 72, and 120 hrs after inoculation. The recombinant human thioredoxin-1 treatment significantly improved the survival rate of H1N1-inoculated mice, although the treatment did not affect virus propagation in the lung. The treatment significantly attenuated the histological changes and neutrophil infiltration in the lung of H1N1-inoculated mice. The treatment significantly attenuated the production of tumor necrosis factor-α and chemokine (C-X-C motif) ligand 1 in the lung and oxidative stress enhancement, which were observed in H1N1-inoculated mice. H1N1 induced expressions of tumor necrosis factor-α and chemokine (C-X-C motif) ligand 1 in murine lung epithelial cells MLE-12, which were inhibited by the addition of recombinant human thioredoxin-1. The recombinant human thioredoxin-1 treatment started 30 mins after H1N1 inoculation also significantly improved the survival of the mice. CONCLUSIONS:: Exogenous administration of recombinant human thioredoxin-1 significantly improved the survival rate and attenuated lung histological changes in the murine model of influenza pneumonia. The protective mechanism of thioredoxin-1 might be explained by its potent antioxidative and anti-inflammatory actions. Consequently, recombinant human thioredoxin-1 might be a possible pharmacological strategy for severe influenza virus infection in humans. © 2013 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. | - |
dc.language | English | - |
dc.title | Redox-active protein Thioredoxin-1 administration ameliorates influenza a virus (H1N1)-induced acute lung injury in mice | - |
dc.type | Article | - |
dc.relation.issue | 1 | - |
dc.relation.volume | 41 | - |
dc.relation.index | SCI | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 171 | - |
dc.relation.lastpage | 181 | - |
dc.relation.journaltitle | Critical Care Medicine | - |
dc.identifier.doi | 10.1097/CCM.0b013e3182676352 | - |
dc.identifier.wosid | WOS:000313150300020 | - |
dc.identifier.scopusid | 2-s2.0-84872082870 | - |
dc.author.google | Yashiro M. | - |
dc.author.google | Tsukahara H. | - |
dc.author.google | Matsukawa A. | - |
dc.author.google | Yamada M. | - |
dc.author.google | Fujii Y. | - |
dc.author.google | Nagaoka Y. | - |
dc.author.google | Tsuge M. | - |
dc.author.google | Yamashita N. | - |
dc.author.google | Ito T. | - |
dc.author.google | Masutani H. | - |
dc.author.google | Yodoi J. | - |
dc.author.google | Morishima T. | - |
dc.contributor.scopusid | Junji Yodoi(35994345400) | - |
dc.date.modifydate | 20220112143825 | - |