Protective effect of allicin on high glucose/hypoxia-induced aortic endothelial cells via reduction of oxidative stress

Abstract

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-κB (NF-κB), NADPH oxidase 4 (Nox4) and hypoxia-inducible factor-1α (HIF-1α) and the activity of PKC were measured using ELISA. A quantitative polymerase chain reaction (qPCR) was adopted to evaluate the mRNA expression of Nox4, HIF-1α and NF-κB. The altered cell morphology observed in HG was notably ameliorated in the AG and GG. The protein levels of 8-OHdG, NF-κB, Nox4, HIF-1α 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-κB, Nox4, HIF-1α 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-1α.

DPP‐4 inhibitors promote proliferation and migration of rat brain microvascular endothelial cells under hypoxic/high‐glucose conditions, potentially through the SIRT1/HIF‐1/VEGF pathway

“…We stimulated rBMVECs with hypoxic/high-glucose conditions by mimicking the diabetic state at a cellular level. 39 Our results indicate that hypoxic and high-glucose culturing resulted in a dramatic inhibition of the proliferative and migratory abilities of rBMVECs, confirming the relationship between diabetic states and endothelial cell dysfunction. 17,40 In response to hypoxia, cells are able to trigger the expression of numerous adaptive genes.…”

“…Here, we selected rat brain microvascular endothelial cells (rBMVECs) to investigate the influence of diabetic states on cell proliferation and migration. We stimulated rBMVECs with hypoxic/high‐glucose conditions by mimicking the diabetic state at a cellular level . Our results indicate that hypoxic and high‐glucose culturing resulted in a dramatic inhibition of the proliferative and migratory abilities of rBMVECs, confirming the relationship between diabetic states and endothelial cell dysfunction …”

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

“…Allicin has been reported to have anti-oxidative and anti-inflammatory effects [27, 28]. In this study, the effects of allicin on LPS-induced vascular injury were investigated.…”

Renin-angiotensin system inhibitor attenuates oxidative stress induced human coronary artery endothelial cell dysfunction via the PI3K/AKT/mTOR pathway

“…The nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) system is the main cellular source of ROS in endothelial cells [10]. Reactive oxygen species play fundamental roles in various signaling pathways under normal physiological conditions [11].…”