Rapamycin Attenuated Cardiac Hypertrophy Induced by Isoproterenol and Maintained Energy Homeostasis via Inhibiting NF-κB Activation

Figure 5

NF-κB participates in the role of Rapa in upregulating fatty acid metabolism in cardiomyocytes induced by isoproterenol. (a) Cytoplasmic proteins extracted from cardiomyocytes were immunoblotted with anti-p-mTOR, mTOR, PPARα, and PGC-1α antibodies. ((b), (c), and (d)) Densitometric analysis of the relative protein expression of the ratio of p-mTOR/mTOR, PPARα, and PGC-1α. And α-tubulin was used to normalize proteins loading. ((d), (e), and (f)) Expression of metabolic genes associated with fatty acid metabolism (PPARα, PGC1α, MCAD, LCAD, CPT-1β, and CPT-2) at mRNA levels. The mRNA was prepared and normalized to β-actin gene. 𝑛=3 experiments in duplicate. Error bars, SD. ^∗𝑃<0.05 versus control group; ^∗∗𝑃<0.01 versus control group; ^∗𝑃<0.001 versus control group; ^#𝑃<0.05 versus model group; and ^#𝑃<0.01 versus model group.

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