Key result
CoQ10 significantly reduced markers of cardiac damage, oxidative stress, energy metabolism, myocardial fibrosis, and apoptosis in mice with doxorubicin-induced heart failure.
Why the study?
Doxorubicin leads to cardiovascular-related side effects, and coenzyme Q10 has been shown to protect against cardiac damage, prompting investigation of its protective effects in mice.
Does CoQ10 prevent cardiac damage in doxorubicin-induced heart failure in C57BL/6 mice?
Does CoQ10 prevent cardiac damage in doxorubicin-induced heart failure in C57BL/6 mice?
p-value: p=<0.01
CoQ10 attenuates doxorubicin-induced cardiotoxicity in mice by reducing oxidative stress, inflammation, fibrosis, and apoptosis.
CoQ10 protection in murine DOX model is hypothesis-generating; leaves open translation to human cardiotoxicity prevention.
BACKGROUND: Cardiovascular disease is associated with high morbidity and mortality. Doxorubicin (DOX) is an effective adjunct to cancer chemotherapy but leads to cardiovascular-related side effects. Because coenzyme Q10 (CoQ10) has been shown to protect against cardiac damage, this study was conducted to investigate the protective effects of CoQ10 against cardiac damage in mice. METHODS: We randomly divided six-week-old male C57BL/6 mice into four groups: control (n = 7), CoQ10 (n = 7), heart failure (HF) (n = 7), and HF+CoQ10 (n = 6) groups. HF group was induced via intraperitoneal injections with DOX (5 mg/kg) once weekly for 4 weeks. CoQ10 was solube in corn oil. The mice of CoQ10 and HF+CoQ10 group were given CoQ10 (100 mg/kg) once a day for 8 weeks. All mice were subjected to different treatment regimens for eight weeks. Metabolic characteristics, cardiac damage, oxidative stress markers (SIRT1, SIRT3, eNOS, TE, P53, SIRT5, CAT, HO-1, and SOD), energy metabolism markers (PARP-1 and PPAR-γ), myocardial fibrosis markers (Smad3 and TGF-β), and apoptosis markers (BAK, BCL-XL, and caspase-8) were analyzed at eight weeks after the different treatments. RESULTS: CoQ10 reduced the levels of molecules related to cardiac damage, oxidative stress, energy metabolism, and myocardial fibrosis in mice with doxorubicin-induced HF. CoQ10 also exerted anti-apoptotic effects in HF mice. CONCLUSIONS: CoQ10 may be useful for preventing cardiac damage in DOX-induced HF.
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Pei et al. (2022) studied Doxorubicin-induced heart failure (n=27). Coenzyme Q10 (CoQ10) vs. Doxorubicin-induced heart failure without CoQ10 was evaluated on Cardiac damage, oxidative stress, energy metabolism, myocardial fibrosis, and apoptosis markers (p=<0.01). CoQ10 significantly reduced markers of cardiac damage, oxidative stress, energy metabolism, myocardial fibrosis, and apoptosis in mice with doxorubicin-induced heart failure.
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