Correction to: Myricitrin Alleviates Oxidative Stress-induced Inflammation and Apoptosis and Protects Mice against Diabetic Cardiomyopathy (Scientific Reports, (2017), 7, 1, (44239), 10.1038/srep44239)

Correction to: Scientific Reportshttps://doi.org/10.1038/srep44239, published online 13 March 2017 This Article contains errors. Due to the errors in figure assembly, the Western blotting results of Akt, Lamin B1 and β-actin are incorrect in Figures 5, 7 and 8. These errors do not change the scientific conclusions of the article. The correct Figure 5 and its accompanying legend appear below. (Figure presented.) Myricitrin exerts cardioprotective effects by activating the PI3K/Akt pathway and Nrf2/ARE signaling. H9c2 cells were pretreated with the PI3K inhibitor LY294002 (50 μ M) for 4 h, and then H9c2 cells pretreated with Myr for 12 h were incubated with AGEs for 36 h. (A) The expression of Akt, p-Akt, GSK-3β, p-GSK-3β, and Nrf2 signaling proteins in H9c2 cells by immunoblotting analysis. Quantitative analysis of the p-Akt/Akt expression level (B), p-GSK-3β / GSK-3β expression level (C), and the statistical analysis of Nrf2, NQO-1 and HO-1 expression levels relative to the control group (D). **p < 0.01 vs the control group; ^##p < 0.01 vs the AGEs group; ^ΔΔp < 0.01 vs the AGEs + Myr group. The correct Figure 7 and its accompanying legend appear below. (Figure presented.) Myr attenuated diabetic myocardial inflammation and promoted expression of Nrf2-mediated anti-oxidative enzymes. (A) The expression of P65, TNF-α, and Nrf2 signaling proteins in the diabetic heart by immunoblotting analysis. (B) IL-6 and TNF-α levels were determined by ELISA. n = 6. The relative expression levels of Cyto-Nrf2, Nucl-Nrf2, NQO-1, and HO-1 (C), as well as P65 and TNF-α relative to β -actin and Lamin B1 (D) were expressed in the bar graphs. **p < 0.01 vs the control group; ^#p < 0.05 and ^##p < 0.01 vs the model group. The correct Figure 8 and its accompanying legend appear below. (Figure presented.) Myr attenuated apoptosis in the diabetic heart through activation of Akt signaling and inhibition of ERK1/2 signaling. (A) Representative images of apoptotic proteins and (B) bar diagrams showing that Myr effectively prevented diabetes-induced apoptosis. (C) The Akt, GSK-3β and ERK phosphorylation were determined by western blotting; densitometric quantification is shown in the bar diagrams (D). (E) Schematic illustration for the prevention of Myr from diabetes/AGEs-induced injury in cardiomyocytes and diabetic mice. n = 3, **p < 0.01 vs the control group; ^#p < 0.05 and ^##p < 0.01 vs the model group.