期刊
WORLD JOURNAL OF HEPATOLOGY
卷 9, 期 34, 页码 1261-1269出版社
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.4254/wjh.v9.i34.1261
关键词
Hepatic ischemia-reperfusion injury; Ischemia reperfusion injury; Warm ischemia-reperfusion injury; Glutaredoxins; Thioredoxins; Electron microscopy; Oxidative stress; Portal triad clamping
资金
- Swedish Cancer society (Cancerfonden)
- Swedish Cancer and Allergy fund (Cancer-och Allergifonden)
AIM To study the effects of warm ischemia-reperfusion (I/R) injury on hepatic morphology at the ultrastructural level and to analyze the expression of the thioredoxin (TRX) and glutaredoxin (GRX) systems. METHODS Eleven patients undergoing liver resection were subjected to portal triad clamping (PTC). Liver biopsies were collected at three time points; first prior to PTC (baseline), 20 min after PTC (post-ischemia) and 20 min after reperfusion (post-reperfusion). Electron microscopy and morphometry were used to study and quantify ultrastructural changes, respectively. Additionally, gene expression analysis of TRX and GRX isoforms was performed by quantitative PCR. For further validation of redox protein status, immunogold staining was performed for the isoforms GRX1 and TRX1. RESULTS Post-ischemia, a significant loss of the liver sinusoidal endothelial cell (LSEC) lining was observed (P = 0.0003) accompanied by a decrease of hepatocyte microvilli in the space of Disse. Hepatocellular morphology was well preserved apart from the appearance of crystalline mitochondrial inclusions in 7 out of 11 patients. Post-reperfusion biopsies had similar features as post-ischemia with the exception of signs of a reactivation of the LSECs. No changes in the expression of redox-regulatory genes could be observed at mRNA level of the isoforms of the TRX family but immunoelectron microscopy indicated a redistribution of TRX1 within the cell. CONCLUSION At the ultrastructural level, the major impact of hepatic warm I/R injury after PTC was borne by the LSECs with detachment and reactivation at ischemia and reperfusion, respectively. Hepatocytes morphology were well preserved. Crystalline inclusions in mitochondria were observed in the hepatocyte after ischemia.
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