[Retracted] Irisin Attenuates Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in the H9C2 Cellular Model of Septic Cardiomyopathy through Augmenting Fundc1-Dependent Mitophagy

Figure 2

Irisin enhances mitochondrial metabolism and ATP production in LPS-stimulated cardiomyocytes through Fundc1-related mitophagy. (a) ELISA analysis shows ATP levels in control, LPS-stimulated, irisin plus LPS-stimulated cardiomyocytes, and irisin plus LPS-stimulated Fundc1-silenced cardiomyocytes. (b, c) ELISA results show activities of mitochondrial complexes I and III in control, LPS-stimulated, irisin plus LPS-stimulated cardiomyocytes, and irisin plus LPS-stimulated Fundc1-silenced cardiomyocytes. (d, e) ELISA results show the levels of (d) glucose and (e) lactic acid in the medium from control, LPS-stimulated, irisin plus LPS-stimulated H9C2 cardiomyocytes, and irisin plus LPS-stimulated Fundc1-silenced cardiomyocytes. denotes vs. PBS group; ^# denotes vs. LPS group; ^@ denotes vs. LPS + irisin.

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