ABSTRACT
Glycogen storage disease type I and glycogenic hepatopathy are the most common type of primary and secondary hepatic glycogenosis, with presenting common radiological features of hepatomegaly, hepatic signal, or density change. Beyond that, glycogen storage disease type I shows hepatocellular adenomas or fatty liver, while glycogenic hepatopathy does not.
Subject(s)
Glycogen Storage Disease Type I/diagnostic imaging , Glycogen/metabolism , Liver Diseases/diagnostic imaging , Liver/diagnostic imaging , Magnetic Resonance Imaging , Tomography, X-Ray Computed , Diagnosis, Differential , Glycogen Storage Disease Type I/metabolism , Humans , Liver/metabolism , Liver Diseases/metabolism , Predictive Value of TestsABSTRACT
PURPOSE: To investigate the effect of metformin on renal tubular epithelial cell apoptosis and inflammation after kidney ischemia/ reperfusion in rats. METHODS: Eighteen SD rats were randomly divided into three groups: Sham (S), Ischemia/reperfusion (I/R), and Metformin (E). Before establishing the I/R model, group E was administered metformin for three days, while groups S and I/R were administered equal volumes of saline. After three days, a right nephrectomy was performed on all groups, after which the left kidneys of groups E and I/R rats were subjected to 45 min renal ischemia. Renal function, histology, and cell apoptosis were assessed. AMPK, pAMPK, COX-2, and Caspase 3 were also detected. RESULTS: Compared to I/R group, Caspase 3 and COX-2 levels were decreased in group E. COX-2, Caspase3 and pAMPK levels were higher in groups E and I/R than in group S. The pAMPK level of group E was higher than that of I/R group, while COX-2 and caspase 3 were lower in group E than they were in the other groups. There was no significant difference between E and I/R groups in AMPK levels. CONCLUSION: Metformin preconditioning attenuated the inflammation caused by ischemia/reperfusion and inhibited the apoptosis of renal tubular epithelial cells.
Subject(s)
Apoptosis/drug effects , Epithelial Cells/drug effects , Ischemic Preconditioning/methods , Kidney/blood supply , Kidney/drug effects , Metformin/pharmacology , Reperfusion Injury/prevention & control , AMP-Activated Protein Kinases/analysis , Animals , Blood Urea Nitrogen , Blotting, Western , Caspase 3/analysis , Creatinine/blood , Cyclooxygenase 2/analysis , Immunohistochemistry , Kidney/pathology , Male , Random Allocation , Rats, Sprague-Dawley , Reproducibility of Results , Time FactorsABSTRACT
PURPOSE:To investigate the effect of metformin on renal tubular epithelial cell apoptosis and inflammation after kidney ischemia/ reperfusion in rats.METHODS:Eighteen SD rats were randomly divided into three groups: Sham (S), Ischemia/reperfusion (I/R), and Metformin (E). Before establishing the I/R model, group E was administered metformin for three days, while groups S and I/R were administered equal volumes of saline. After three days, a right nephrectomy was performed on all groups, after which the left kidneys of groups E and I/R rats were subjected to 45 min renal ischemia. Renal function, histology, and cell apoptosis were assessed. AMPK, pAMPK, COX-2, and Caspase 3 were also detected.RESULTS:Compared to I/R group, Caspase 3 and COX-2 levels were decreased in group E. COX-2, Caspase3 and pAMPK levels were higher in groups E and I/R than in group S. The pAMPK level of group E was higher than that of I/R group, while COX-2 and caspase 3 were lower in group E than they were in the other groups. There was no significant difference between E and I/R groups in AMPK levels.CONCLUSION:Metformin preconditioning attenuated the inflammation caused by ischemia/reperfusion and inhibited the apoptosis of renal tubular epithelial cells.
Subject(s)
Animals , Male , Apoptosis/drug effects , Epithelial Cells/drug effects , Ischemic Preconditioning/methods , Kidney/blood supply , Kidney/drug effects , Metformin/pharmacology , Reperfusion Injury/prevention & control , AMP-Activated Protein Kinases/analysis , Blood Urea Nitrogen , Blotting, Western , /analysis , Creatinine/blood , /analysis , Immunohistochemistry , Kidney/pathology , Random Allocation , Rats, Sprague-Dawley , Reproducibility of Results , Time FactorsABSTRACT
To investigate the effect of metformin on renal tubular epithelial cell apoptosis and inflammation after kidney ischemia/ reperfusion in rats. Eighteen SD rats were randomly divided into three groups: Sham (S), Ischemia/reperfusion (I/R), and Metformin (E). Before establishing the I/R model, group E was administered metformin for three days, while groups S and I/R were administered equal volumes of saline. After three days, a right nephrectomy was performed on all groups, after which the left kidneys of groups E and I/R rats were subjected to 45 min renal ischemia. Renal function, histology, and cell apoptosis were assessed. AMPK, pAMPK, COX-2, and Caspase 3 were also detected. Compared to I/R group, Caspase 3 and COX-2 levels were decreased in group E. COX-2, Caspase3 and pAMPK levels were higher in groups E and I/R than in group S. The pAMPK level of group E was higher than that of I/R group, while COX-2 and caspase 3 were lower in group E than they were in the other groups. There was no significant difference between E and I/R groups in AMPK levels. Metformin preconditioning attenuated the inflammation caused by ischemia/reperfusion and inhibited the apoptosis of renal tubular epithelial cells.(AU)