Key result
Curcumin activation of the Nrf2/HO-1 signaling pathway exerted myocardial protection by reducing ROS formation, increasing cardiomyocyte viability, and inhibiting apoptosis in diabetic cardiomyopathy.
Why the study?
Hyperglycemia contributes to diabetic cardiomyopathy via excess myocardial ROS, but the mechanism of Nrf2 signaling in HG-induced DCM remains unclear.
Does curcumin reduce ROS formation and improve cardiomyocyte viability in in vitro and in vivo models of diabetic cardiomyopathy?
Population
HG pretreated H9c2 cells and high fat-diet, STZ induced Type 2 diabetic rat model
Comparison
Curcumin and shRNA-Nrf2 treatment
Design
In vitro and in vivo preclinical study
Authors
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Preclinical protection in diabetic cardiomyopathy models leaves open clinical translation and human trials.
Does curcumin reduce ROS formation and improve cardiomyocyte viability in in vitro and in vivo models of diabetic cardiomyopathy?
Curcumin protects against diabetic cardiomyopathy injury by activating the Nrf2/HO-1 signaling pathway and reducing reactive oxygen species.
Wu et al. (2022) studied Diabetic cardiomyopathy. Curcumin was evaluated on ROS formation, cardiomyocyte viability, and apoptosis. Curcumin activation of the Nrf2/HO-1 signaling pathway exerted myocardial protection by reducing ROS formation, increasing cardiomyocyte viability, and inhibiting apoptosis in diabetic cardiomyopathy.
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