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Exendin-4 attenuates high glucose-induced cardiomyocyte apoptosis via inhibition of endoplasmic reticulum stress and activation of SERCA2a

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Our results showed a significant increase in intracellular GSH content in cells treated with 100 M of -EC, GSH, or UDE containing 100 M -EC, compared to the untreated control cells (Fig

Bettelli E, Carrier Y, Gao W, Korn T, Strom TB, Oukka M, et al

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However, when the balance between ROS production and antioxidant defenses (e.g., superoxide dismutase (SOD) and glutathione peroxidase (GPx)) is disrupted, oxidative stress occurs