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ISRN Anesthesiology
Volume 2011 (2011), Article ID 510297, 7 pages
http://dx.doi.org/10.5402/2011/510297
Research Article

Xenon Upregulates Hypoxia Inducible Factor 1 Alpha in Neonatal Rat Brain under Normoxic Conditions

1Department of Physiology and Biochemistry, School of Medicine, University of Pisa, Pisa, Italy
2Department of Anesthesiology, University of Texas Medical School at Houston, 6431 Fannin Street, Houston, TX 77030, USA
3Division of Surgical Molecular and Ultrastructural Pathology, School of Medicine, University of Pisa, Pisa, Italy
4The Anaesthetics, Pain Medicine, and Intensive Care Section, Department of Surgery and Cancer, Imperial College London, Chelsea & Westminster Hospital, London, UK
5Surgical Pathology Unit, Department of Oncology, ASL no. 1, Massa-Carrara, Italy

Received 20 October 2011; Accepted 9 November 2011

Academic Editors: J.-H. Baumert and C.-T. Wu

Copyright © 2011 Simona Valleggi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Xenon can induce cell and organ protection through different molecular mechanisms related to oxygen level. We explored the effect of xenon on oxygen-related signalling in the central nervous system via hypoxia inducible factor 1 alpha (HIF-1α) and mammalian target of rapamycin (mTOR). Methods. Postnatal day 7 (P7) Sprague Dawley rats were exposed to 25% oxygen/75% nitrogen (air group) or 25% oxygen/75% xenon (treatment group) for 120 min. Brains were collected immediately (transcript analysis—relative real-time polymerase chain reaction) or 24 hours (protein analysis—immunohistochemistry) after the 120-minute exposure period; peak anesthetic preconditioning has been previously identified at 24 hours post-exposure. Results. HIF-1α transcript and protein levels were found to be increased in xenon-exposed compared to air-exposed brains. Sustained nuclear translocation of the protein, accounting for an increased activity of HIF-1α, was also noted. mTOR transcript analysis revealed no significant difference between xenon-exposed and air-exposed brains immediately after the 120-minute exposure. Conclusion. Our data suggest that xenon induces the upregulation of HIF-1α transcription and translation, which may contribute to xenon's neuroprotective preconditioning effect. However, given that xenon exposure did not affect mTOR transcription, further investigation into other signalling cascades mediating xenon’s effects on HIF-1α in developing brain is warranted.