Key result
Pterostilbene protected cardiomyocytes from acute doxorubicin exposure-induced oxidative stress and mitochondrial damage via PGC1α upregulation and deacetylation through activating AMPK and SIRT1 cascades.
Why the study?
Does pterostilbene prevent doxorubicin-induced acute cardiotoxicity and mitochondrial oxidative stress in preclinical models?
Does pterostilbene prevent doxorubicin-induced acute cardiotoxicity and mitochondrial oxidative stress in preclinical models?
p-value: p=<0.05
Pterostilbene protects against acute doxorubicin-induced cardiotoxicity in preclinical models by reducing oxidative stress and mitochondrial damage via the AMPK/SIRT1-PGC1α pathway.
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Pterostilbene may attenuate DOX cardiotoxicity via AMPK/SIRT1 in vitro; leaves open clinical translation pending in vivo trials.
Liu et al. (2019) studied Doxorubicin-induced acute cardiotoxicity (n=75). Pterostilbene vs. Doxorubicin alone was evaluated on Myocardial injury, oxidative stress, and mitochondrial morphological disorder (p=<0.05). Pterostilbene protected cardiomyocytes from acute doxorubicin exposure-induced oxidative stress and mitochondrial damage via PGC1α upregulation and deacetylation through activating AMPK and SIRT1 cascades.
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