Research Paper Volume 12, Issue 16 pp 16224—16237

SirT3 activates AMPK-related mitochondrial biogenesis and ameliorates sepsis-induced myocardial injury

Figure 5. Inhibition of mitochondrial biogenesis decreases SirT3-mediated mitochondrial protection and cardiomyocyte survival. (A, B) ELISA assay was used to analyze mitochondrial electron transport chain complex activity in the presence of LPS. Lentivirus-loaded SirT3 (SirT3-OE) was incubated with cardiomyocytes in the presence of LPS. Compound C (CC), an antagonist of AMPK, was used to inhibit the activation of AMPK in SirT3-OE–treated cardiomyocytes. (C, D) Immunofluorescence of mitochondrial ROS production. (E, F) TUNEL staining of apoptotic cardiomyocytes. SirT3-OE was incubated with cardiomyocytes in the presence of LPS. CC was used to inhibit the activation of AMPK in SirT3-OE–treated cardiomyocytes. Then, the number of TUNEL-positive cardiomyocytes was determined. (G) ELISA was used to detect the activity of caspase-3. *P < 0.05.