Key result
Rosiglitazone completely abolished the significant increase in ROS production induced by 10 mmol/L glucose in HUVECs through an AMPK-dependent and PPARgamma-independent mechanism.
Why the study?
Does rosiglitazone reduce glucose-induced oxidative stress in human umbilical vein endothelial cells?
Does rosiglitazone reduce glucose-induced oxidative stress in human umbilical vein endothelial cells?
Rosiglitazone protects endothelial cells against glucose-induced oxidative stress via an AMPK-dependent and PPARgamma-independent mechanism.
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Hypothesis-generating for AMPK-mediated endothelial protection in vitro; leaves open clinical translation in hyperglycemia.
Ceolotto et al. (2007) studied Glucose-induced oxidative stress. Rosiglitazone vs. High glucose without rosiglitazone was evaluated on Intracellular ROS production and NAD(P)H oxidase/AMPK activities. Rosiglitazone completely abolished the significant increase in ROS production induced by 10 mmol/L glucose in HUVECs through an AMPK-dependent and PPARgamma-independent mechanism.
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