Key result
Neopetroside-B reduced doxorubicin-induced cardiac fibrosis and improved cardiac function in a xenograft mouse model, while impairing cancer cell viability.
Why the study?
Cumulative doses of the chemotherapy drug doxorubicin cause mitochondrial dysfunction, leading to acute or chronic cardiotoxicity.
Does Neopetroside-B prevent doxorubicin-induced cardiotoxicity in preclinical models?
Does Neopetroside-B prevent doxorubicin-induced cardiotoxicity in preclinical models?
Answers are grounded in this paper and cite their sources.
Neopetroside-B demonstrates potential as a cardioprotective agent against doxorubicin-induced cardiotoxicity while maintaining anticancer effects in preclinical models.
Doxorubicin, a member of the anthracycline family, is a widely prescribed anticancer chemotherapy drug. Unfortunately, cumulative doses of doxorubicin can cause mitochondrial dysfunction, leading to acute or chronic cardiotoxicity. This study demonstrated that Neopetroside-B (NPS-B) protects cardiomyocytes in the presence of doxorubicin. NPS-B improved mitochondrial function in cardiomyocytes by increasing ATP production and oxygen consumption rates. On the other hand, NPS-B negatively influenced cancer cell lines by increasing reactive oxygen species. We analyzed NPS-B-influenced metabolites (VIP > 1.0; AUC>0.7; p < 0.05) and proteins (FC > 2.0) and constructed metabolite-protein enrichment, which showed that NPS-B affected uracil metabolism and NAD-binding proteins (e.g., aldehyde dehydrogenase and glutathione reductase) in cardiomyocytes. However, for the cancer cells, NPS-B decreased the NAD+/NADH balance, impairing cell viability. In a xenograft mouse model treated with doxorubicin, NPS-B reduced cardiac fibrosis and improved cardiac function. NPS-B may be a beneficial intervention to reducing doxorubicin-induced cardiotoxicity with anticancer effects.
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Yoon et al. (2023) studied Doxorubicin-induced cardiotoxicity. Neopetroside-B (NPS-B) was evaluated on Cardiac fibrosis and cardiac function. Neopetroside-B reduced doxorubicin-induced cardiac fibrosis and improved cardiac function in a xenograft mouse model, while impairing cancer cell viability.
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