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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 624819, 8 pages
Research Article

Neuroprotective Effect of Ulinastatin on Spinal Cord Ischemia-Reperfusion Injury in Rabbits

1Department of Anesthesiology, The 2nd People’s Hospital of Guangdong Province, Guangdong Provincial Emergency Hospital, Guangzhou 510317, China
2Department of Anesthesiology, Huizhou Municipal Central Hospital, Huizhou 516001, China
3Department of Anesthesiology, The First People’s Hospital of Shangqiu, Shangqiu 476000, China
4Department of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang 524003, China
5Department of Anesthesiology, The University of Hong Kong, Hong Kong

Received 17 September 2014; Revised 8 January 2015; Accepted 8 January 2015

Academic Editor: Mengzhou Xue

Copyright © 2015 Bingbing Liu 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.


Ulinastatin (UTI), a trypsin inhibitor, is isolated and purified from human urine and has been shown to exert protective effect on myocardial ischemia reperfusion injury in patients. The present study was aimed at investigating the effect of ulinastatin on neurologic functions after spinal cord ischemia reperfusion injury and the underlying mechanism. The spinal cord IR model was achieved by occluding the aorta just caudal to the left renal artery with a bulldog clamp. The drugs were administered immediately after the clamp was removed. The animals were terminated 48 hours after reperfusion. Neuronal function was evaluated with the Tarlov Scoring System. Spinal cord segments between L2 and L5 were harvested for pathological and biochemical analysis. Ulinastatin administration significantly improved postischemic neurologic function with concomitant reduction of apoptotic cell death. In addition, ulinastatin treatment increased SOD activity and decreased MDA content in the spinal cord tissue. Also, ulinastatin treatment suppressed the protein expressions of Bax and caspase-3 but enhanced Bcl-2 protein expression. These results suggest that ulinastatin significantly attenuates spinal cord ischemia-reperfusion injury and improves postischemic neuronal function and that this protection might be attributable to its antioxidant and antiapoptotic properties.