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Fig. 2 | Cell & Bioscience

Fig. 2

From: Dapagliflozin attenuates hypoxia/reoxygenation-caused cardiac dysfunction and oxidative damage through modulation of AMPK

Fig. 2

Dapagliflozin (DAPA) prevents the upregulation of ROS via AMPK/ PKC/ NADPH oxidase signaling.

Representative Western blot images (a) and relative densitometric bar graphs of Nox-2/Na/K ATPase (b) and Rac-1/Na/K ATPase (c) in H9c2 cells exposed to hypoxia for 1 h and reoxygenation for 4 h (H1R4) were shown. Protein expression levels of Nox-2 and β-actin in ventricular tissue from sham control, ischemia/reperfusion (I/R), and I/R plus DAPA treatment animals (d, e), eight animals in each group, were examined. Activity of NADPH oxidase in H9c2 cells (f) and primary cardiomyocytes (g) was measured. ROS generation was measured using a flow cytometry to examine the fluorescent intensity of H9c2 cells (h) and primary cardiomyocytes (i). For in vitro experiments, the data were presented as the mean ± SD of three biological replicates at three separate times. (* indicating p < 0.05 compared with the control group; # indicating p < 0.05 compared to H1R4 condition or I/R without DAPA treatment; & indicating p < 0.05 compared with the DAPA-treated cells in H1R4 condition)

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