Key result
Kirenol protects H9c2 cells from doxorubicin-induced apoptosis and oxidative stress via IGF-IR and Nrf2 pathways.
Why the study?
Despite reported benefits of kirenol, its cardiac effects have not been clarified, particularly regarding doxorubicin-induced cardiotoxicity and oxidative stress.
Does Kirenol prevent doxorubicin-induced apoptosis and hypertrophy in H9c2 cells?
Population
H9c2 cells
Comparison
KRL treatment vs DOX alone
Design
In vitro laboratory study
Authors
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Supports kirenol as potential cardioprotectant in vitro; leaves open translation to clinical doxorubicin cardiotoxicity prevention.
Does Kirenol prevent doxorubicin-induced apoptosis and hypertrophy in H9c2 cells?
Kirenol demonstrates potential as a cardio-protective agent against doxorubicin-induced cardiotoxicity in vitro by activating the PI3K/AKT and Nrf2 signaling pathways and suppressing apoptosis.
Alzahrani et al. (2021) studied Doxorubicin-induced cardiac hypertrophy. Kirenol (KRL) vs. Doxorubicin (DOX) was evaluated on Cellular apoptosis and oxidative stress. Kirenol protected H9c2 cells against doxorubicin-induced apoptosis and oxidative stress by activating the IGF-IR-dependent p-PI3K/p-AKT and Nrf2 signaling pathways.