Role of leukotrienes on hepatic ischemia/reperfusion injury in rats
Role of leukotrienes on hepatic ischemia/reperfusion injury in rats
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DOI：
10.1016/j.jss.2003.07.004
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发表时间：
2004-06-01
影响因子：
2.2
通讯作者：
Tanaka, M
中科院分区：
文献类型：
--
作者：
Takamatsu, Y;Shimada, K;Tanaka, M
背景由半胱氨酰LT（cLT; LTC 4、LTD 4和LTE 4）和LTB 4组成的白三烯（LT）是增强血管通透性和中性粒细胞募集的有效脂质介质，这是肝缺血/再灌注（I/R）损伤的共同特征。本研究的目的是探讨LT是否可以介导肝I/R后的肝和肺损伤。材料和方法。对Sprague-Dawley大鼠进行90分钟的部分肝缺血，然后进行3、12和24小时的再灌注。在肝和肺组织中，测定LT含量和LT合成酶、5-脂氧合酶（5LO）、LTC 4合酶（LTC 4-S）和LTA（4）水解酶（LTA（4）-H）的mRNA表达。通过血浆ALT、组织学检查和湿干组织重量比评估组织损伤。结果。再灌注12和24 h后肝组织中的cLT含量增加4- 5倍，与对照组相比，这伴随着肝水肿和血浆ALT升高的增强。两种组织中LT合成酶的mRNA表达均无显著变化。LTB 4水平没有增加，尽管在两种组织中有显著的中性粒细胞浸润。这些数据表明，cLT在再灌注期间在肝脏中产生，并且可能有助于肝水肿的发展并发挥细胞毒性。LTB 4以外的因素可能导致中性粒细胞浸润。(C)2004年爱思唯尔公司All rights reserved.
Background. Leukotrienes (LT), composed of cysteinyl LT (cLT; LTC4, LTD4, and LTE4) and LTB4, are potent lipid mediators enhancing the vascular permeability and recruitment of neutrophils, which are common features of hepatic ischemia/reperfusion (I/R) injury. The aim of this study was to investigate whether LT can mediate the liver and lung injuries following hepatic I/R.Materials and methods. Sprague-Dawley rats were subjected to 90 min of partial hepatic ischemia followed by 3, 12, and 24 h of reperfusion. In the hepatic and pulmonary tissues, LT content and the mRNA expression of LT-synthesis enzymes, 5-lypoxygenase (5LO), LTC4 synthase (LTC4-S), and LTA(4) hydrolase (LTA(4)-H) were measured. Tissue injuries were assessed by plasma ALT, histological examination, and wet-to-dry tissue weight ratios.Results. The cLT content in the hepatic tissue after 12 and 24 h reperfusion was increased 4- to 5-fold compared to controls and this was accompanied by the enhancement of hepatic edema and plasma ALT elevation. There were no significant changes in the mRNA expression of LT-synthesis enzymes in both tissues. LTB4 levels were not increased despite a significant neutrophil infiltration in both tissues.Conclusions. These data suggest that cLT are generated in the liver during the reperfusion period and may contribute to the development of hepatic edema and exert cytotoxicity. Factors other than LTB4 may contribute to neutrophil infiltration. (C) 2004 Elsevier Inc. All rights reserved.