Effects of Radiation and High Glucose on Endothelial Dysfunction: an in vitro study

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Endothelium is highly radiosensitive, multifunctional, and is the main component of the blood vessel wall. Both radiation and hyperglycaemia could cause endothelial dysfunction, which is the primary injury of radiation-induced and non-radiation-induced carotid atherosclerosis in post-radiotherapy (RT) head and neck carcinoma patients and diabetes patients, respectively. Commonly, some post-RT patients have diabetes simultaneously, leading them to suffer from the accumulative effects of radiation and hyperglycaemia. However, the underlying mechanisms of individual and combined effects of radiation and hyperglycaemia have not been revealed. Human umbilical vein endothelial cells (HUVECs) were used in the study to investigate the individual and combined effects of radiation and high glucose level on endothelial dysfunction in vitro, and possible signalling pathways involved. The cell viability, tube formation and protein levels, including nitric oxide synthesis (NOS), angiogenesis-related [focal adhesion kinase (FAK), vascular endothelial growth factors receptor (VEGFR)], and apoptosis (caspase-3)-related proteins at high/low glucose level combined with 0/8 Gy of radiation were being evaluated. Our findings suggested that radiation suppressed endothelial cell viability (p<0.001), and the combined effects of radiation and high glucose-induced higher angiogenesis of endothelial cells. eNOS-mediated and FAK-mediated signalling transductions are the possible signalling pathways involved in radiation- and hyperglycaemia-induced endothelial dysfunction.

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