Study On Selenocytine Immobilization On TiO Surface And Nitric Oxide Released Inhibit Endothelial Cells Injury Induced By Oxiadative Stress

Endothelial dysfunction is an important initial event at the onset of atherosclerosis which following oxidative stress.The nitric oxide(NO)catalyzed by materials may affect the growth,adhesion,proliferation,and other behavior of endothelial cells.In this paper,a series of surfaces with stable catalytic release of nitric oxide were constructed on the titanium oxide film surface,and NO with different release rates were released from RSNO catalyzed by L-selenocystine,thereby realized good endothelial cell compatibility on sample surface.Hydrogen peroxide was used to damage endothelial cells to simulate oxidative stress,and effect of material catalytic NO release on endothelial cells in peroxidation injury was studied.SEM,AFM,XPS were used to characterize the modified material surface.The results showed that the polydopamine layer was deposited successfully,and L-selenocystine was successfully grafted to the sample,and the amount of L-selenocystine on 5-Se sample was slightly higher than 3-Se and 8-Se sample.After L-selenocystine immobilized,the surface roughness of the sample was decreased.The water contact angle results showed that the effect of grafting L-selenocysteine on the hydrophilic and hydrophobic on the material surface was not significant.The results of the QCM-D showed that the amount of L-selenocystine adsorbed on the 5-layer polydopamine surface by chemical and physical effects was far greater than that of the 3-layer polydopamine sample.Amino quantification results indicated that the amount of amino groups increaseed as the number of polydopamine layers increaseed.Catalyzing NO donor to release NO experimental results showed that the Se-containing samples could stably catalyze RSNO to release NO sustainably and 5-Se sample had the highest NO release rate.The static endothelial cells culture results showed that the number of adhered endothelial cell and the migration distance on TiO films was more than that of samples without nitric oxide donor.when NO donor was added,adhesion number and migration distance of endothelial cells on all sample surface were increased,and the number of endothelial cells on the surface of Se-containing samples was more,especially on the surface of 5-Se sample had the most amount of endothelial cell adhesion and the longest migration distance of endothelial cell.Using hydrogen peroxide to damage endothelial cells simulate oxidative stress.Through the screening concentration experiments,it was found that the activity of endothelial cells had been reduced about 50% at a concentration of 200?M.Therefore,the peroxide microenvironment of atherosclerotic lesions was simulated with 200?M hydrogen peroxide.The AO/PI staining results showed that the apoptosis cells gradually appeared When hydrogen peroxide was added.But under the condition of pretreatment with NO donor,the cell apoptosis rate decreased,and with the increase of NO release rate,the apoptosis rate decreased.Endothelial cells treated with 5-Se sample had higher cell activity.Catalytic chamber experiment results showed that pretreatment with NO donor could enhance the NO secretion ability of endothelial cells after hydrogen peroxide injury,and it increased with the increase of NO release rate.All the above results showed that within a certain release rate range,the materials catalytic release of the stable and sustained NO can increase the activity of endothelial cells and promote the proliferation,adhesion and migration of endothelial cells..In the state of oxidative stress,the materials catalytic release NO can alleviate the endothelial peroxide-induced damage caused by hydrogen peroxide.