Abstract
Objective To evaluate the relationship between endoplasmic reticulum stress and cell apoptosis during liver cold ischemia-reperfusion(I/R)in rats. Methods Thirty-two SPF healthy adult male Sprague-Dawley rats, weighing 200-250 g, were divided into 2 groups(n=16 each)using a random number table: sham operation group(group S)and liver cold I/R group(group I/R). In group I/R, the liver was perfused through the portal vein with 4 ℃ lactated Ringer's solution 6-8 ml/min for 30 min after liver ischemia, and the liver blood flow was restored after the end of perfusion. At 6 h of reperfusion in group I/R or at 6 h after peritoneum closure in group S, blood samples from the inferior vena cava were collected for determination of serum alanine transaminase and aspartate transaminase concentrations. After blood sampling, liver tissues were obtained for examination of pathological changes and for determination of malondialdehyde content(by thiobarbituric acid method), superoxide dismutase activity(using xanthine oxidase method), cell apoptosis(using TUNEL), expression of endoplasmic reticulum protein 46(ERP46), immunoglobulin heavy chain binding protein(BiP)and caspase-12(by immunohistochemistry), and expression of ERP46, BiP and caspase-12 mRNA(using quantitative real-time polymerase chain reaction). The pathological changes were scored. Apoptosis rate was calculated. Results Compared with group S, the serum alanine transaminase and aspartate transaminase concentrations, pathological scores, malondialdehyde content and apoptosis rate were significantly increased, the activity of superoxide dismutase was decreased, and the expression of ERP46, BiP and caspase-12 protein and mRNA was up-regulated in group I/R(P<0.05). Conclusion The mechanism of cell apoptosis during liver cold I/R may be related to excessive activation of endoplasmic reticulum stress in rats. Key words: Endoplasmic reticulum; Stress; Reperfusion injury; Liver transplantation
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