Key result
HSP-17 peptide protected H9c2 cardiomyocytes against doxorubicin-induced oxidative stress and apoptosis by activating the PI3K/Akt pathway.
Why the study?
Oxidative stress and apoptosis drive doxorubicin-induced myocardial injury, and HSP-17, low-expressed in doxorubicin-treated mouse heart tissue, is predicted to confer myocardial protection.
Does HSP-17 peptide prevent doxorubicin-induced oxidative stress and apoptosis in H9c2 cardiomyocytes?
Population
H9c2 cardiomyocyte model of doxorubicin-induced cytotoxicity
Comparison
HSP-17 peptide vs doxorubicin alone and with LY294002
Design
In vitro controlled laboratory study
Authors
Loading...
Hypothesis-generating for HSP-17 in doxorubicin cardiotoxicity; leaves open clinical translation.
Does HSP-17 peptide prevent doxorubicin-induced oxidative stress and apoptosis in H9c2 cardiomyocytes?
The novel peptide HSP-17 protects H9c2 cardiomyocytes against doxorubicin-induced oxidative stress and apoptosis by activating the PI3K/Akt pathway, suggesting a potential therapeutic target for doxorubicin-induced myocardial injury.
Chen et al. (2022) studied Doxorubicin-induced myocardial injury. HSP-17 peptide vs. Doxorubicin alone was evaluated on Cell viability, LDH level, ROS, and cardiomyocyte apoptosis. HSP-17 peptide protected H9c2 cardiomyocytes against doxorubicin-induced oxidative stress and apoptosis by activating the PI3K/Akt pathway.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: