Abstract | BACKGROUND: Myocardial cell injury and cardiac myocyte apoptosis are associated with sepsis. Glutamine (Gln) has been reported to repair myocardial cell injury. The aim of this study was to explore the role of Gln on cardiac myocytes in a cecal ligation and puncture (CLP) model of sepsis in Wistar rats. MATERIALS AND METHODS: RESULTS: Rat cardiac myocyte damage induced by CLP was reduced by Gln treatment and Hsp90 overexpression, and these changes were reversed by Hsp90 knockdown. Bcl-2 expression, Bcl-2-associated X protein, p53, p53 upregulated modulator of apoptosis, caspase-8, caspase-9, and caspase-3 activities were significantly upregulated in the CLP model, which were reduced by Gln treatment and Hsp90 overexpression. CONCLUSIONS: Gln reduced apoptosis of cardiac myocytes in a rat model of sepsis, by promoting Hsp90 expression. Further studies are needed to determine the possible therapeutic action of Gln in sepsis in human tissue.
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Authors | Wanxia Li, Shaoyu Tao, Qinghua Wu, Tao Wu, Ran Tao, Jun Fan |
Journal | The Journal of surgical research
(J Surg Res)
Vol. 220
Pg. 247-254
(12 2017)
ISSN: 1095-8673 [Electronic] United States |
PMID | 29180187
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2017 Elsevier Inc. All rights reserved. |
Chemical References |
- HSP90 Heat-Shock Proteins
- Glutamine
- Caspases
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Topics |
- Animals
- Apoptosis
- Caspases
(metabolism)
- Disease Models, Animal
- Glutamine
(metabolism)
- HSP90 Heat-Shock Proteins
(metabolism)
- Myocytes, Cardiac
(physiology)
- Rats, Wistar
- Sepsis
(metabolism, pathology)
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