Brief Reports
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 1, 2004; 10(9): 1375-1378
Published online May 1, 2004. doi: 10.3748/wjg.v10.i9.1375
Protective effect of doxorubicin induced heat shock protein 72 on cold preservation injury of rat livers
Hao Chen, Ying-Yan Yu, Ming-Jun Zhang, Xia-Xing Deng, Wei-Ping Yang, Jun Ji, Cheng-Hong Peng, Hong-Wei Li
Hao Chen, Xia-Xing Deng, Wei-Ping Yang, Cheng-Hong Peng, Hong-Wei Li, Department of Surgery and Center of Organ Transplantation, Ruijin Hospital, Shanghai Second Medical University, Shanghai 200025, China
Ying-Yan Yu, Jun Ji, Center of Organ Transplantation, Ruijin Hospital, Shanghai Second Medical University, Shanghai 200025, China
Ming-Jun Zhang, Animal Laboratory, Ruijin Hospital, Shanghai Second Medical University, Shanghai 200025, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Hao Chen, Department of Surgery and Center of Organ Transplantation, Ruijin Hospital, Shanghai Second Medical University, Shanghai 200025, China. chenhaodr@sohu.com
Telephone: +86-21-64370045 Fax: +86-21-64333548
Received: August 26, 2003
Revised: October 1, 2003
Accepted: October 22, 2003
Published online: May 1, 2004
Abstract

AIM: To observe the protective effect of heat shock protein 72 (HSP 72) induced by pretreatment of doxorubicin (DXR) on long-term cold preservation injury of rat livers.

METHODS: Sprague-Dawley rats were administered intravenously DXR at a dose of 1 mg/kg body mass in DXR group and saline in control group. After 48 h, the rat liver was perfused with cold Linger’s and University of Wisconsin (UW) solutions and then was preserved in UW solution at 4 °C for 24, 36 and 48 h. AST, ALT, LDH and hyaluronic acid in preservative solution were determined. Routine HE, immunohistochemical staining for HSP 72 and electron microscopic examination of hepatic tissues were performed.

RESULTS: After 24, 36 and 48 h, the levels of AST, ALT and hyaluronic acid in preservative solution were significantly higher in control group than in DXR group (P < 0.05), while LDH level was not significantly different between the 2 groups (P > 0.05). Hepatic tissues in DXR group were morphologically normal and significantly injured in control group. HSP 72 was expressed in hepatocytes and sinusoidal endothelial cells in DXR group but not in control group.

CONCLUSION: Pretreatment of DXR may extend the time of rat liver cold preservation and keep liver alive. The expression of HSP 72 in liver can prevent hepatocytes and sinusoidal endothelial cells from long-term cold preservation injury.

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