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

Figure 3

Activation of TGR5 induces the Nrf2/HO-1 pathway in mouse cardiomyocytes. (a) Nuclear extracts were prepared from cardiomyocytes treated with INT-777 (30 μM) at the indicated time points to detect Nrf2 protein by immunoblotting. (b) Cells were treated with 30 μM INT-777 for the indicated times to detect HO-1 by immunoblotting. (c) Cells were infected with TGR5 shRNA adenoviral particles for 48 h or pretreated with 100 μM SQ22536 (cAMP Inhibitor) for 3 h and then treated 30 μM INT-777 for 2 h. Proteins (20 μg) from nuclear (N) fractions were subjected to immunoblotting. (d) Cells were infected with Nrf2 shRNA lentiviral particles for 48 h. Proteins from cell lysates were subjected to immunoblotting. (e) Cells were infected with TGR5 or Nrf2 shRNA viral particles for 48 h or pretreated with 100 μM SQ22536 for 3 h and then treated with 30 μM INT-777 for 6 h. Proteins from cell lysates were subjected to immunoblotting. Data are expressed as the of three independent experiments. vs. 0 h or control; ^# vs. HG.

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