Pathogenic Factors Of Diabetes Mellitus Induce The Damage And Alteration Of Adhesive Function Of Vascular Endothelial Cells

Vascular complications are critical lethal cause of the patients with diabetes mellitus and basis of complication is the damage of vasscular endothelial cells. Using various methods, we investigated the damage mechanisms of cultured human umibilical vein endothelial cells (HUVEC) stimulated by experimental hyperglycemia (HG), hyperinsulinemia (HI), hyperproinsulinemia (HPI) and TNF-α on cellular and molecular level in vitro. The purpose of the research is to clear the part of pathogenesis and pathophysiological mechanisms. I. Observation of the expression of α_v β₃ on HUVEC. 1. Performed on the level of membrane protein.Using the methods of Enzyme Linked Immunosorbent Assay (ELISA),membranous receptor-antibody and nuclear DNA double fluorescence labeling, we observed the expressional change of adhensive receptor-integrin (α_v β₃ )on the surface of HUVEC exposed to HG, HI and TNF a and found that these agents could up-regulate the expression of α_v β₃ .The kinetic curves of ELISA, concentration- and time-density curves, show the pattern that HG, HI and TNF α enhance the α_v p 3 expression was concentration- and time-dependent within certain range. Density of α_v β₃ was reduced and the cells was injured with over-dosage or longer-time in some degree.The results of fluorescent-immunohistochemistry demonstrate the ifference between the cultured and suspended ECs in the expression of α_v β₃ The average fluorescent density of the suspended HUVEC was higher than that of the cultured cells. The reason for it may be that α_v β₃ of suspended cells was more exposed or redistributed.With the receptor over-expression on the surface of HUVEC, it was observed that fluorescent denisty of the nuclear DNA was higher in experimental groups than that of control group with...