Changes of sphingolipids profiles after ischemia-reperfusion injury in the rat liver

Background Hepatic ischemia-reperfusion (I/R) injury occurs in many clinical procedures. The molecular mechanisms responsible for hepatic I/R injury however remain unknown. Sphingolipids, in particular ceramide, play a role in stress and death receptor-induced hepatocellular death, contributing to t...

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Veröffentlicht in:Chinese medical journal 2009-12, Vol.122 (24), p.3025-3031
Hauptverfasser: Zhai, Shu-Ting, Liu, Guang-Yi, Xue, Fei, Sun, Gong-Ping, Liang, Liang, Chen, Wei, Xu, Guo-Dong, Li, Jun-Jian, Yang, Jun, Liang, Ting-Bo
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Sprache:eng
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Zusammenfassung:Background Hepatic ischemia-reperfusion (I/R) injury occurs in many clinical procedures. The molecular mechanisms responsible for hepatic I/R injury however remain unknown. Sphingolipids, in particular ceramide, play a role in stress and death receptor-induced hepatocellular death, contributing to the progression of several liver diseases including liver I/R injury. In order to further define the role of sphingolipids in hepatic I/R, systemic analysis of sphingolipids after reperfusion is necessary. Methods We investigated the lipidomic changes of sphingolipids in a rat model of warm hepatic I/R injury, by delayed extraction matrix-assisted laser desorption ionization time-of-flight mass spectrometry (DE MALDI-TOF-MS). Results The total amounts of ceramide and sphingomyelin and the intensity of most kinds of sphingolipids, mainly sphingomyelin, significantly increased at 1 hour after reperfusion (P 〈0.05) and reached peaks at 6 hours after reperfusion (P 〈0.01) compared to controls. Six new forms of ceramide and sphingomyelins appeared 6 hours after reperfusion, they were (m/z) 537.8, 555.7, 567.7, 583.8, 683.5 and 731.4 respectively. A ceramide-monohexoside (m/z) 804.4 (CMH(d18:1C22:1+Na)+) also increased after reperfusion and correlated with extent of liver injury after reperfursion. Conclusions Three main forms of sphingolipids, ceramide, sphingomyelin and ceramide-monohexoside, are related to hepatic I/R injury and provide a new perspective in understanding the mechanisms responsible for hepatic I/R injury.
ISSN:0366-6999
2542-5641
DOI:10.3760/cma.j.issn.0366-6999.2009.24.022