Rapamycin Attenuated Cardiac Hypertrophy Induced by Isoproterenol and Maintained Energy Homeostasis via Inhibiting NF-κB Activation
Figure 2
Rapa maintained energy homeostasis and inhibited NF-κB activation in hypertrophied hearts induced by isoproterenol. (a) The ultrastructures of the mitochondria were analyzed under TEM. Transmission electron micrographs of histological sections from the apex of left ventricle with different treatments were shown. Black arrows indicate disorganized cristae and vacuoles of mitochondria in the hypertrophied hearts. White arrows indicate autophagosomes. Scale bars, 1 μm. (b) State III and state IV respiration rates. (c) Respiratory control rate (RCR) was calculated as the ratio of state III respiration rates to state IV respiration rates. Values represented as mean ± SD of 6 rats in each group. (d) ATP production. Values represented as mean ± SD of 6 rats in each group. (e) Expression of metabolic genes associated with fatty acid metabolism at mRNA levels. The mRNA was prepared and normalized to β-actin gene. Values represented as mean ± SD of 4 to 5 rats in each group. ((f) and (h)) Cytoplasmic and nuclear extracts from left ventricles of three groups of rats were immunoblotted with anti-p65 and anti-IκB-α antibodies. ((g) and (i)) Densitometric analysis of the relative protein expression of p65 and IκB-α. Histone H3 and α-tubulin were used to normalize the nuclear and cytosolic proteins loading, respectively. Values represented as mean ± SD of 4 to 5 rats in each group. Model, the cardiac hypertrophy model induced by isoproterenol; Rapa, isoproterenol-infused rats treated with Rapa. versus control group; versus control group; versus model group; and versus model group.
