Effects Of Perfluorocarbon On Hypoxia/reoxygenation Injury Of Human Umbilical Vein Endothelial Cells

Objective Establishing hypoxic / reoxygenation( H / R) injury model, and then investigating the protective effect and the regulation mechanism of Perfluocarbon(PFC) on Human umbilical vein endothelial cells(HUVECs) in the model of hypoxia/reoxygenation injury. To provide a more objective and adequate theoretical basis for the PFC’s clinical application in the myocardial ischemia-reperfusion injury, through the observe of PFC’s biological effects and mechanism.Methods H/R models were established by sodium hydrosulfite, and the experiment was divided into 6 groups: control group, PFC group with PFC at a 10% volume, H/R group, PFC+H/R treatment group(the volume ratios of culture medium were 5%, 10%, 20%).The cell viability was detected by CCK-8 method. The contents of malondialdehyde(MDA),nitric oxide(NO) and the activities of superoxide dismutase(SOD) in cells, as well as the lactate dehydrogenase(LDH) in the culture medium, were measured by biochemistry approaches. The expression of apoptosis-related protein Caspase-3 was analyzed by Western blotting(WB).Results Compared with the control group, every detected indexes of 10%PFC group had no statistical significance(P > 0.05). Compared with the model group, 10% and 20%PFC treatment groups could increase the cell viability A, decrease the content of NO and reduce Caspase-3 expression(P < 0.05); Every PFC treatment group could significantly reduce the release of LDH and the contents of MDA, and also increase the activities of SOD(P < 0.01).Conclusion(1) Hypoxia / reoxygenation injury can cause the occurrence of intracellular oxidative stress, and then lead to the appearance of necrosis and apoptosis;(2) PFC has a significant protective effect on HUVECs in the injury of HR, and its mechanism may be related to the inhibition of oxidative stress and inflammation so that enhance the cells ability of antioxidant and anti-apoptotic.