Key result
Peptide Szeto-Schiller 31 ameliorated doxorubicin-induced cardiotoxicity in vitro and in vivo by inhibiting the p38 MAPK signaling pathway, reducing reactive oxygen species, and decreasing apoptosis.
Why the study?
Oxidative stress drives doxorubicin-induced cardiotoxicity, but the role of the antioxidant peptide Szeto-Schiller 31 in this condition remains unclear.
Does peptide SS31 ameliorate doxorubicin-induced cardiotoxicity in preclinical models?
Population
H9c2 cells and C57BL/6 mice with doxorubicin-induced cardiotoxicity
Comparison
SS31 vs control in DOX models
Design
In vitro and in vivo preclinical study
Authors
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SS31 attenuates doxorubicin cardiotoxicity in animals; leaves open clinical translation and human efficacy.
Does peptide SS31 ameliorate doxorubicin-induced cardiotoxicity in preclinical models?
p-value: p=<0.05
Peptide SS31 ameliorates doxorubicin-induced cardiotoxicity in preclinical models by inhibiting the p38 MAPK signaling pathway, suggesting its potential as a cardioprotective therapeutic agent.
Zhang et al. (2021) studied Doxorubicin-induced cardiotoxicity (n=48). Peptide Szeto-Schiller 31 (SS31) vs. Doxorubicin alone or vehicle was evaluated on Cardioprotective effect (cardiac function, ROS levels, apoptosis, and fibrosis) (p=<0.05). Peptide Szeto-Schiller 31 ameliorated doxorubicin-induced cardiotoxicity in vitro and in vivo by inhibiting the p38 MAPK signaling pathway, reducing reactive oxygen species, and decreasing apoptosis.
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