Key result
Glutathione protects against doxorubicin-induced cardiotoxicity in preclinical models by reducing ROS and regulating pERK signaling.
Why the study?
This study investigated the protective effect of glutathione against doxorubicin-induced cardiotoxicity.
Does glutathione protect against doxorubicin-induced cardiotoxicity in human cardiac progenitor cells and in vivo models?
Does glutathione protect against doxorubicin-induced cardiotoxicity in human cardiac progenitor cells and in vivo models?
Glutathione demonstrates potential as a therapeutic strategy to mitigate doxorubicin-induced cardiotoxicity through ROS reduction and pERK signal regulation.
Glutathione may protect against doxorubicin cardiotoxicity in preclinical models; hypothesis-generating and requires human trials before any clinical consideration.
This study investigated the protective effect of glutathione (GSH), an antioxidant drug, against doxorubicin (DOX)-induced cardiotoxicity. Human cardiac progenitor cells (hCPCs) treated with DOX (250 to 500 nM) showed increased viability and reduced ROS generation and apoptosis with GSH treatment (0.1 to 1 mM) for 24 h. In contrast to the 500 nM DOX group, pERK levels were restored in the group co-treated with GSH and suppression of ERK signaling improved hCPCs' survival. Similarly to the previous results, the reduced potency of hCPCs in the 100 nM DOX group, which did not affect cell viability, was ameliorated by co-treatment with GSH (0.1 to 1 mM). Furthermore, GSH was protected against DOX-induced cardiotoxicity in the in vivo model (DOX 20 mg/kg, GSH 100 mg/kg). These results suggest that GSH is a potential therapeutic strategy for DOX-induced cardiotoxicity, which performs its function via ROS reduction and pERK signal regulation.
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Lee et al. (2023) studied Doxorubicin-induced cardiotoxicity. Glutathione (GSH) vs. Doxorubicin alone was evaluated on Cell viability, ROS generation, apoptosis, and in vivo cardiotoxicity. Glutathione co-treatment protected against doxorubicin-induced cardiotoxicity in human cardiac progenitor cells and an in vivo model by reducing ROS generation and regulating pERK signaling.
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