Apoptosis after Ischemia-Reperfusion Injury in Rat Liver.
- Author:
Tae Yun KIM
1
;
Won Seok LEE
;
Ik Jin YUN
;
Sung Kyu PARK
;
Dae Sik HONG
;
Yun Soo KIM
;
Chan Sup SHIM
;
Min Hyuck LEE
;
Jae Jun KIM
Author Information
1. Department of Surgery, Soon Chun Hyang University, College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
rat liver;
ischemia-reperfusion injury;
apoptosis
- MeSH:
Animals;
Apoptosis*;
Cell Death;
Cytoplasm;
Fibrosis;
Free Radicals;
Hepatic Artery;
Hepatocytes;
Humans;
Ischemia;
Liver Transplantation;
Liver*;
Male;
Microscopy;
Necrosis;
Oxygen;
Portal Vein;
Rats*;
Rats, Sprague-Dawley;
Reperfusion;
Reperfusion Injury*
- From:Korean Journal of Hepato-Biliary-Pancreatic Surgery
2000;4(2):9-17
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Liver ischemia-reperfusion injury is one of the major problems in liver transplantation and radical liver surgery. Ischemia-reperfusion injury is known to be induced by oxygen free radicals and the cell damages used to result in cell necrosis. However, apoptosis, another type of cell death, may be also related to the ischemia-reperfusion injury and hepatic dysfunction after ischemia-reperfusion injury may also be associated with the apoptosis. We examined the correlation between ischemiareperfusion injury and apoptosis in rat liver by apoptosis morphological study. METHODS: Male Sprague-Dawley rats were used. For each rats, 60 minutes partial clamp was applied to the hepatic artery and portal vein. Then, 5 groups which had 4 rats each were divided on the base of reperfusion injury duration of 0, 1, 3, 6, 24 hour (total numbers of rat were 20). For each rat, the central lobe which was given ischemic injury (ischemic groups) and the lateral lobe which was not given ischemic injury (control groups) were sampled after 60 minutes ischemia time. Apoptosis was examined by the method of TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay. Counter staining was H&E staining and under the light microscopy with x60 and x300 magnification, apoptotic cell were examined. RESULTS: The groups of apoptotic cells were observed in 24hr reperfusion group. In 24 hr groups, besides conglomeration of apoptotic cells destructed hepatocyte cytoplasms were also observed. In all of the non-ischemic control group, no apoptosis was observed. Although the early reperfusion groups had not so much apoptotic cells as 24 hour group, the number of apoptotic cells in 0, 1, 3, 6 was significantly increased compared with the control groups. CONCLUSION: Apoptosis activity may be increased during reperfusion period with the maximum in 24 hour. This meant that apoptosis in ischemia-reperfusion injury might be associated with the chronic damage to hepatocyte and it might be the one of the causes of fibrosis or cirrhosis mechanism.
