Shikonin protects H9C2 cardiomyocytes against hypoxia/reoxygenation injury through activation of PI3K/Akt signaling pathway - 11/06/18
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Highlights |
• | SHK pretreatment significantly increased cell viability, attenuated LDH release, and suppressed cardiomyocyte apoptosis induced by H/R exposure. |
• | SHK pretreatment restored the loss of mitochondrial membrane potential (MMP) and cytochrome c release in H/R-treated H9C2 cells. |
• | SHK significantly enhanced the phosphorylation of Akt and GSK-3β in H/R-treated H9C2 cells. |
• | The beneficial effects of SHK in H/R-treated H9C2 cells were partially reversed by LY294002, a specific PI3K/Akt inhibitor. |
Abstract |
Myocardial ischemic/reperfusion (I/R) injury often leads to irreversible myocardial cell death and even heart failure, with limited therapeutic possibilities. In the present study, we evaluated the protective effects of shikonin (SHK) against hypoxia/reoxygenation (H/R)-induced cardiomyocyte damage and explored the underlying mechanisms. H9C2 cardiomyocytes were pretreated with different doses of SHK prior to H/R exposure. We observed that SHK pretreatment significantly increased cell viability, attenuated LDH release, and suppressed cardiomyocyte apoptosis induced by H/R exposure. SHK pretreatment also restored the loss of mitochondrial membrane potential (MMP) and cytochrome c release. In addition, SHK significantly enhanced the phosphorylation of Akt and GSK-3β in H/R-treated H9C2 cells. These protective effects of SHK were partially reversed by LY294002, a specific PI3K/Akt inhibitor. Therefore, our findings suggested that SHK might be a promising agent for myocardial I/R injury, and PI3K/Akt signaling plays a crucial role during this process.
Le texte complet de cet article est disponible en PDF.Keywords : Shikonin, H9C2 cells, Hypoxia/reoxygenation injury, Viability, Mitochondria-dependent apoptosis, PI3K/Akt signaling
Plan
Vol 104
P. 712-717 - août 2018 Retour au numéro
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