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

Figure 2

Activation of TGR5 reduces the HG-induced increase in the expression of proinflammatory cytokines and NF-κB signaling in mouse cardiomyocytes. (a) 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 with 30 μM INT-777 (selective TGR5 agonist) for 3 h, followed by addition of HG to cardiomyocytes for a further 6 h. Proteins (20 μg) from cell lysates or nuclear (N) fractions were subjected to immunoblotting. (b) Cells were infected with TGR5 shRNA adenoviral particles for 48 h or pretreated with 100 μM SQ22536 for 3 h and then treated with 30 μM INT-777 for 3 h or 30 μM JSH-23 (NF-κB inhibitor) for 1 h, followed by exposure to HG for a further 2 h (TNF-α) or 8 h (IL-1β and IL-6). IL-1β, IL-6, and TNF-α mRNA expression was determined by RT-PCR. Data are expressed as the of three independent experiments. vs. control; ^# vs. HG; ^& vs. HG+INT-777.

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