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FK506可改善与缺血相关的肝损伤。

FK 506 ameliorates the hepatic injury associated with ischemia.

作者信息

Sakr M F, Hassanein T I, Zetti G M, Van Thiel D H

机构信息

Department of Surgery, University of Pittsburgh, PA 15261.

出版信息

Life Sci. 1990;47(8):687-91. doi: 10.1016/0024-3205(90)90623-y.

Abstract

Ischemic damage of the allograft liver is a major problem in clinical liver transplantation. Therefore the identification of hepatoprotective agents is a high priority at most liver transplantation programs. FK 506, a potent new immunosuppressive agent has been reported to possess hepatotrophic activity. To evaluate the putative hepatotrophic activity of FK 506 on experimental hepatic ischemia, rats were subjected to a subtotal hepatectomy following experimental ischemia and subsequent rat survival was assessed. FK 506 (0.3 mg/Kg) administered intravenously 24 hours prior to the induction of hepatic ischemia, reduced the subsequent mortality rate from 100% among controls given saline to only 20% (P less than 0.001). This observation demonstrates that FK 506 enhances the regenerative response of the liver to ischemic injury and may, in addition to its immunologic activity have hepatotrophic activity as well.

摘要

同种异体移植肝的缺血性损伤是临床肝移植中的一个主要问题。因此,在大多数肝移植项目中,确定肝脏保护剂是当务之急。FK 506是一种新型强效免疫抑制剂,据报道具有肝营养活性。为了评估FK 506对实验性肝缺血的假定肝营养活性,对大鼠进行实验性缺血后行肝次全切除术,并评估随后的大鼠存活率。在诱导肝缺血前24小时静脉注射FK 506(0.3mg/kg),使随后的死亡率从给予生理盐水的对照组的100%降至仅20%(P<0.001)。这一观察结果表明,FK 506增强了肝脏对缺血性损伤的再生反应,并且除了其免疫活性外,可能还具有肝营养活性。

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