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• W2960293062 endingPage "109143" @default.
• W2960293062 startingPage "109143" @default.
• W2960293062 abstract "Araloside C (AsC) has potential cardioprotective properties. However, the underlying mechanism of AsC-mediated cardioprotection, especially the role of mitochondrial function, remains largely unknown. Here, we used H9c2 cardiomyocytes to study the cardioprotective mechanisms of AsC through H2O2-induced oxidative stress. Cell viability, lactate dehydrogenase release, mitochondrial functions and bioenergetics were evaluated. Western blot analysis was used to measure the protein expression levels of apoptosis and the phosphorylation of AMP-activated protein kinase (AMPK). Results revealed that AsC increased cell viability, improved mitochondrial membrane potential disruption, decreased mitochondrial reactive oxygen species level, elevated cellular ATP levels and alleviated impaired mitochondrial respiration in H2O2-induced H9c2 cardiomyoblasts injury. Furthermore, AsC modulated apoptosis-associated protein expression and AMPK pathway in H9c2 cells under oxidative stress. In conclusion, AsC potentially protects H9c2 cardiomyoblasts against oxidative stress by regulating mitochondrial function and AMPK activation. AsC may be an effective therapeutic agent for the prevention of oxidative stress in cardiac injury." @default.
• W2960293062 created "2019-07-23" @default.
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• W2960293062 date "2019-09-01" @default.
• W2960293062 modified "2023-10-04" @default.
• W2960293062 title "Araloside C protects H9c2 cardiomyoblasts against oxidative stress via the modulation of mitochondrial function" @default.
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• W2960293062 doi "https://doi.org/10.1016/j.biopha.2019.109143" @default.
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