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Dynamic expression of hepatic thioredoxin mRNA in rats with non-alcoholic fatty liver disease.
Journal of Digestive Diseases 2010 April
OBJECTIVE: To investigate the expression and significance of thioredoxin messenger ribonucleic acid (mRNA) in the development of non-alcoholic fatty liver disease (NAFLD) induced by a high fat diet.
METHODS: A total of 48 male Wistar rats were divided into a normal control group and a model group, which were both divided into three subgroups (at weeks 9, 13 and 18, respectively). The levels of serum tumor necrosis factor-alpha (TNF-alpha), free fatty acid (FFA), total cholesterol (TC) and triglyeride (TG), changes in the serum and hepatic tissue superoxide dismutase (SOD), reduced glutathione hormone (GSH) and malondialdehyde (MDA) were measured. The expression of thioredoxin mRNA in rat livers were detected with reverse transcriptase polymerase chain reaction (RT-PCR). Meanwhile, the pathological changes of liver tissue were observed by hematoxylin-eosin stain.
RESULTS: Simple fatty liver was observed in model group at week 9. From weeks 13 to 18, liver histopathology showed steatohepatitis. Compared with corresponding normal groups, in the model groups the levels of TNF-alpha, FFA, TC, TG in serum, and MDA in serum and liver increased significantly, while the vitality of SOD and GSH content in serum and liver decreased remarkably. Meanwhile, in the model group, the expression of hepatic thioredoxin mRNA was significantly decreased at week 9 compared with the normal group (P < 0.01), then increased gradually, but were lower than the corresponding normal groups at all times (P < 0.01).
CONCLUSION: The expression of thioredoxin mRNA is significantly lower in the liver of rats with NAFLD and might reach the lowest point after developing simple fatty liver. Meanwhile the downregulation of thioredoxin mRNA may cause the inflammatory injury initially in NAFLD.
METHODS: A total of 48 male Wistar rats were divided into a normal control group and a model group, which were both divided into three subgroups (at weeks 9, 13 and 18, respectively). The levels of serum tumor necrosis factor-alpha (TNF-alpha), free fatty acid (FFA), total cholesterol (TC) and triglyeride (TG), changes in the serum and hepatic tissue superoxide dismutase (SOD), reduced glutathione hormone (GSH) and malondialdehyde (MDA) were measured. The expression of thioredoxin mRNA in rat livers were detected with reverse transcriptase polymerase chain reaction (RT-PCR). Meanwhile, the pathological changes of liver tissue were observed by hematoxylin-eosin stain.
RESULTS: Simple fatty liver was observed in model group at week 9. From weeks 13 to 18, liver histopathology showed steatohepatitis. Compared with corresponding normal groups, in the model groups the levels of TNF-alpha, FFA, TC, TG in serum, and MDA in serum and liver increased significantly, while the vitality of SOD and GSH content in serum and liver decreased remarkably. Meanwhile, in the model group, the expression of hepatic thioredoxin mRNA was significantly decreased at week 9 compared with the normal group (P < 0.01), then increased gradually, but were lower than the corresponding normal groups at all times (P < 0.01).
CONCLUSION: The expression of thioredoxin mRNA is significantly lower in the liver of rats with NAFLD and might reach the lowest point after developing simple fatty liver. Meanwhile the downregulation of thioredoxin mRNA may cause the inflammatory injury initially in NAFLD.
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