Cucurbitacin I Protects H9c2 Cardiomyoblasts against H2O2‐Induced Oxidative Stress via Protection of Mitochondrial Dysfunction Article Swipe
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· 2018
· Open Access
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· DOI: https://doi.org/10.1155/2018/3016382
· OA: W2792197657
Cucurbitacin I, a triterpenoid natural compound, exhibits various pharmacological properties, including anticancer, anti‐inflammatory, and hepatoprotective properties. However, antioxidant effects of cucurbitacin I in cardiac cells are currently unknown. In the present study, we assessed the preventive effects of cucurbitacin I against the oxidative stress in H9c2 cardiomyoblasts. To evaluate antioxidant effects of cucurbitacin I in H9c2 cardiomyoblasts, H 2 O 2 ‐treated H9c2 cells were pretreated with various concentrations of the cucurbitacin I. Cell viability, reactive oxygen species (ROS) production, and apoptosis were determined to elucidate the protective effects of cucurbitacin I against H 2 O 2 ‐induced oxidative stress in H9c2 cells. In addition, we assessed the mitochondrial functions and protein expression levels of mitogen‐activated protein kinases (MAPKs). Cucurbitacin I prevented the cells against cell death and ROS production and elevated the antioxidant protein levels upon oxidative stress. Furthermore, cucurbitacin I preserved the mitochondrial functions and inhibited the apoptotic responses in H 2 O 2 ‐treated cells. Cucurbitacin I also suppressed the activation of MAPK proteins (extracellular signal‐regulated kinase 1/2, c‐Jun N‐terminal kinase, and p38). Collectively, cucurbitacin I potentially protects the H9c2 cardiomyoblasts against oxidative stress and further suggests that it can be utilized as a therapeutic agent for the prevention of oxidative stress in cardiac injury.
