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Ubiquinol-cytochrome c reductase core protein 1 may be involved in delayed cardioprotection from preconditioning induced by diazoxide.

Ubiquinol-cytochrome c reductase core protein 1 may be involved in delayed cardioprotection from preconditioning induced by diazoxide.
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Long Z, Duan G, Li H, Yi T, Wu X, Chen F, Wu Z, Gao Y,


Long Z, Duan G, Li H, Yi T, Wu X, Chen F, Wu Z, Gao Y, (click to view)

Long Z, Duan G, Li H, Yi T, Wu X, Chen F, Wu Z, Gao Y,

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PloS one 2017 07 2712(7) e0181903 doi 10.1371/journal.pone.0181903
Abstract

This study aimed to use long-term diazoxide treatment to establish a loss-of-cardioprotection model and then perform proteomics analysis to explore which proteins of mitochondrial inner membrane (MIM) are potentially involved in delayed cardioprotection. Rats received 1 to 8 weeks of diazoxide treatments (20 mg•kg-1•d-1) to establish a loss-of-cardioprotection model in different groups. Detection of serum cTnI levels and cell apoptosis assays in heart tissue were performed. Then, rats MIM after 0, 4 and 6 weeks of diazoxide treatment was isolated and proteomics analysis was performed. An invitro model of H9C2 cells was performed to explore the effects of targeted protein on delayed cardioprotection. The effect of delayed cardioprotection by diazoxide preconditioning disappeared when diazoxide treatments were given for six weeks or longer. Ubiquinol-cytochrome c reductase core protein 1 (UQCRC1) was identified in the proteomics analysis. UQCRC1 expression was upregulated by diazoxide treatment in H9C2 cells, and UQCRC1 down-regulation could increase the lactate dehydrogenase release and apoptosis rate after injury induced by oxygen glucose deprivation. These results showed that UQCRC1 might contribute to the loss-of-cardioprotection model induced by long-term diazoxide treatment and play a role in delayed cardioprotection.

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