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| Protective effects of N-acetylcysteine on brain-dead rat liver |
| Shui-Jun Zhang, Ting-Wu Ma, Xiu-Xian Ma, Jian-Jun Gou, Ji-Hua Shi and Wen-Zhi Guo |
Zhengzhou, China
Author Affiliations: Department of Hepatobiliary Surgery (Zhang SJ, Ma XX and Gou JJ), and Department of Transplantation Surgery (Ma TW, Shi JH and Guo WZ), First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China
Corresponding Author: Shui-Jun Zhang, MD, Department of Hepatobiliary Surgery, First Affiliated Hospital, Zhengzhou University, Zhengzhou 450052, China (Tel: 86-371-66913032; Fax: 86-371-66989954; Email: zhangshuijun@medmail.com.cn) |
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Abstract BACKGROUND: Brain-dead donors have been the main sources in organ transplantation. But many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liver injury after brain-death in rats and the protective effects of N-acetyleysteine (NAC) on liver injury.
METHODS: A total of 30 Wistar rats were randomized into 3 groups: normal control group (C), brain-dead group (B), and NAC pretreatment group (N). At 4 hours after the establishment of a brain-dead model, serum was collected to determine the levels of ALT, AST, TNF-α and hyaluronic acid (HA). Hepatic tissue was obtained for electron microscopic examination.
RESULTS: At 4 hours, the levels of ALT, AST, TNF-α, and HA in group N were significantly higher than those in group C, but these parameters were significantly lower than those in group B. Electron microscopy showed activated Kupffer cells, denuded sinusoidal endothelial cells (SECs), and widened fenestration in group B, but eliminated activation of Kupffer cells and intact SECs in group N.
CONCLUSION: Brain death can cause liver injury, and N-acetyleysteine can protect the liver from the injury.
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2006, Vol. 5 
