Activation of TGR5 Partially Alleviates High Glucose-Induced Cardiomyocyte Injury by Inhibition of Inflammatory Responses and Oxidative Stress

Figure 4

Effect of TGR5 activation on HG-induced oxidative stress in mouse cardiomyocytes. (a, b) ROS production was detected by flow cytometry with DCFH-DA staining at 20 min after INT-777 treatment. ROS levels were calculated as fold changes relative to no treatment (0 μM). (c, d) Changes in ROS production were detected by flow cytometry with DCFH-DA staining. Cells were infected with TGR5 shRNA adenoviral particles for 48 h, or cells were pretreated with 10 μM ZnPP for 1 h and then treated with INT-777 for 3 h, followed by addition of HG to cells for a further 12 h. ROS levels were calculated as fold changes relative to the control. (e, f) Immunoblotting for the expression of Nrf2 and HO-1 in cells. Cells were treated with INT-777 for 3 h, followed by addition of HG to cells for a further 12 h. Data are expressed as the of three independent experiments. vs. control; ^# vs. HG; vs. HG+INT-777.

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