Реферат: 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.

Библиографическая ссылка: Yoon C.S. , Nifantiev N.E. , Yashunsky D.V. , Kim H.K. , Han J.
Neopetroside-B alleviates doxorubicin-induced cardiotoxicity via mitochondrial protection
Biomedicine & Pharmacotherapy. 2023. V.165. 115232 . DOI: 10.1016/j.biopha.2023.115232 WOS Scopus OpenAlex

Идентификаторы БД:

≡ Web of science:	WOS:001047240200001
≡ Scopus:	2-s2.0-85166042959
≡ OpenAlex:	W4385387362

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