Résumé
Objective To explore the potential impact of low concentration of metformin on the morphology and function of mitochondria of HepG2 cells. Methods HepG2 cells in experimental group and control group were treated with or without low concentration of metformin (1mM/L), respectively. The cells were incubated for 12h in the incubator with constant temperature and humidity as well as 1% oxygen. Orange Mitoview was used to stain the mitochondria to detect the effects of the drug on its morphology and quantity. Transmission electron microscope was utilized to observe the effect of metformin on the ultrastructure of mitochondria. The mitochondrial respiratory chain complex I activity in HepG2 cell was detected by Complex I Enzyme Activity Dipstick Assay Kit (DAK). Results Orange Mitoview staining showed that low concentration of metformin had little effect on the morphology and number of mitochondria of cells in experimental group , and the difference between control and experimental group was not statistically significant (P > 0.05). In addition, the result was further determined by transmission electron microscopy. However, DAK analysis showed that complex I activity of cells in experimental group was significantly lower than that in control group. Conclusion Under Hypoxia conditions, low concentration of metformin had no significant effect on the morphology and number of mitochondria of HepG2 cells, but it significantly reduces the activity of mitochondria of HepG2 cells.
Résumé
Objective This study was carried out to investigate the effect of myocardial insulin resistance on expression of p38 mitogen-activated protein kinase (MAPK) in ischemic heart failure in rat.Methods Male sprague-dawley rats were subjected either to ligation of the left anterior descending artery (LAD) (n =24) or to sham operation (n =24).After two weeks,cardiac size and function were determined by echocardiography.Glucose and fatty acid (FAO) oxidation rates as well as insulin response were measured in the isolated working heart.The protein expression of p38MAPK was evaluated by Western blotting.Results The infarcted hearts were dilated and had a reduced ejection fraction (ejection fraction ＜0.50).The basal glucose oxidation was preserved,but the fatty acid oxidation was significantly reduced.Insulin effect on substrate oxidation was significantly impaired for both the decrease in fatty acid oxidation and the increase in glucose oxidation.The protein expression of p38MAPK in infracted hearts wasfisigni cantly reduced(P＜0.05).Condusion Myocardial infarction in rats caused partial insulin resistance at the level of substrate oxidation,which was associated with cardiac contractile dysfunction and the expression of p38MAPK.