Prevention of hepatic ischemia/reperfusion injury by prolonged delivery of nitric oxide to the circulating blood in mice
Prevention of hepatic ischemia/reperfusion injury by prolonged delivery of nitric oxide to the circulating blood in mice
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DOI：
10.1097/tp.0b013e31815e902b
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发表时间：
2008-01-27
期刊：
影响因子：
6.2
通讯作者：
Hashida, Mitsuru
中科院分区：
文献类型：
--
作者：
Katsumi, Hidemasa;Nishikawa, Makiya;Hashida, Mitsuru
背景为了保护小鼠肝细胞免受缺血/再灌注损伤，通过静脉推注聚乙二醇（PEG）偶联牛血清白蛋白（BSA）（PEG-poly SNO-BSA）来延长一氧化氮（NO）向肝脏的递送。通过阻断门静脉和肝动脉15 min，然后再灌注6 h，在小鼠中诱导肝缺血/再灌注损伤。每一个NO供体在再灌注开始前以2 μ mol NO/kg的剂量注入尾静脉。缺血再灌注导致血浆丙氨酸氨基转移酶和天冬氨酸氨基转移酶活性显著升高。S-亚硝基-N-乙酰青霉胺和NO-BSA，两个经典的S-亚硝基硫醇，没有统计学上显着的效果，在防止标记物的升高。PEG-聚SNO-BSA与PEG-聚SNO-BSA相比，
Background. To protect hepatocytes from ischemia/reperfusion injury in mice, prolonged delivery of nitric oxide (NO) to the liver was performed by a bolus intravenous injection of polyethylene glycol (PEG)-conjugated bovine serum albumin (BSA) with about 10 NO molecules attached via an S-nitrosothiol linkage (PEG-poly SNO-BSA).Methods. A hepatic ischemia/reperfusion injury was induced in mice by occluding the portal vein and the hepatic artery for 15 min followed by 6 hours of reperfusion. Each NO donor was injected into the tail vein just before the initiation of the reperfusion at a dose of 2 mu mol NO/kg.Results. The ischemia followed by reperfusion resulted in a striking increase in plasma alanine aminotransferase and aspartate aminotransferase activities. S-nitroso-N-acetyl penicillamine and NO-BSA, two classical S-nitrosothiols, had no statistically significant effect in preventing elevation of the markers. In marked contrast, PEG-poly SNO-BSA significantly (P