Journal
EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 10, Issue 4, Pages 1394-1400Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2015.2708
Keywords
oxidative stress; allicin; NADPH oxidase 4; hypoxia-inducible factor-1 alpha; 8-hydroxydeoxyguanosine
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This study was designed to explore the protective effect of allicin on aortic endothelial cell injury induced by high glucose/hypoxia and to investigate the corresponding mechanisms. The primary-cultured murine aortic endothelial cells were subcultured. The third passage of cells was adopted and randomly divided into five groups: The normal group (NG), the mannitol group (MG), the high-glucose/hypoxia group (HG), the allicin group (AG) and the protein kinase C (PKC) inhibitor group (GG). The general morphology was observed under an inverted phase-contrast microscope and cell viability was assessed using the MTT assay. Intracellular reactive oxygen species (ROS) levels in the endothelial cells were quantified using dihydroethidium staining. The levels of 8-hydroxydeoxyguanosine (8-OHdG), nuclear factor-kappa B (NF-kappa B), NADPH oxidase 4 (Nox4) and hypoxia-inducible factor-la (HIP-la) and the activity of PKC were measured using ELISA. A quantitative polymerase chain reaction (qPCR) was adopted to evaluate the mRNA expression of Nox4, HIP-la and NF-kappa B. The altered cell morphology observed in HG was notably ameliorated in the AG and GG. The protein levels of 8-OHdG, NF-kappa B, Nox4, HIP-la and PKC in the HG were higher than those in the other groups. Furthermore, the cell viability in the AG was significantly increased and the protein levels of 8-OHdG, NF-kappa B, Nox4, HIP-la and PKC were significantly decreased compared with those in the HG. The ROS production was found to be increased in the HG cells, while there was a significant decrease in the AG cells. These data indicate that allicin exerts a protective effect against high glucose/hypoxia-induced injury in aortic endothelial cells through its antioxidative action, which may involve the inhibition of the PKC pathway and regulation of HIF-1 alpha.
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