Effect of ulinastatin antagonist on ischemia-reperfusion injury of liver
LI Dechu
Abstract
LI Dechu
Abstract
Objective To investigate the pathogenesis of hepatic ischemic-reperfusion (I/R) injury and observe the protection of ulinastatin on the liver. Methods Thirty-eight patients with hepatorrhexis undertaken hepatic hilum occlusion were selected. All patients were randomly divided into I/R group and ulinastatin group. Serum levels of tumor necrosis factor (TNF),malondialdehyde (MDA),aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were tested. The hepatic morphological changes were observed and the number of infiltrated neutrophil in liver tissue at 60 minutes of reperfusion was counted. Results Serum levels of TNF,MDA,AST and ALT in the I/R group were significantly higher than those in the ulinastatin group. Under light microscopy, neutrophils infiltration of liver tissue increased significantly, and electronic microscopic revealed that the hepatic sinusoidal endothelial cells and the hepatocellular mitochondria were injured in the I/R group. Pre_treatment with ulinastatin was able to significantly improved the pathological changes and decreased the hepatic I/R injury. Conclusion Hepatic I/R induce to release TNF-α,liver tissue is protected effectively from I/R injury by the ulinastatin pre_treatment.
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Objective To investigate the pathogenesis of hepatic ischemic-reperfusion (I/R) injury and observe the protection of ulinastatin on the liver. Methods Thirty-eight patients with hepatorrhexis undertaken hepatic hilum occlusion were selected. All patients were randomly divided into I/R group and ulinastatin group. Serum levels of tumor necrosis factor (TNF),malondialdehyde (MDA),aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were tested. The hepatic morphological changes were observed and the number of infiltrated neutrophil in liver tissue at 60 minutes of reperfusion was counted. Results Serum levels of TNF,MDA,AST and ALT in the I/R group were significantly higher than those in the ulinastatin group. Under light microscopy, neutrophils infiltration of liver tissue increased significantly, and electronic microscopic revealed that the hepatic sinusoidal endothelial cells and the hepatocellular mitochondria were injured in the I/R group. Pre_treatment with ulinastatin was able to significantly improved the pathological changes and decreased the hepatic I/R injury. Conclusion Hepatic I/R induce to release TNF-α,liver tissue is protected effectively from I/R injury by the ulinastatin pre_treatment.
Key concepts: Ulinastatin, Medicine, Malondialdehyde, Tumor necrosis factor alpha, Reperfusion injury, Pathology, Necrosis, Gastroenterology