作者: R. Shurtz-Swirski , S. Sela , A. T. Herskovits , S. M. Shasha , G. Shapiro
关键词: Angiopathy 、 Medicine 、 Blood plasma 、 Oxidative stress 、 Diabetes mellitus 、 Necrosis 、 Type 2 diabetes 、 Endocrinology 、 Internal medicine 、 Endothelial dysfunction 、 Inflammation
摘要: OBJECTIVE — To determine the extent to which peripheral polymorphonuclear leukocytes (PMNs) contributed oxidative stress (OS) and inflammation in type 2 diabetic patients. RESEARCH DESIGN AND METHODS PMNs and plasma were separated from blood withdrawn from 18 patients 16 age- and sex-matched normal control subjects. The rate of superoxide release from phorbol 12-myristate 13-acetate (PMA)-stimulated plasma glutathione (GSH) levels served as measures OS. Inflammation was assessed by PMN recruitment, expressed by peripheral counts, vitro survival PMNs, reflects cell necrosis. RESULTS PMA-stimulated diabetes released superoxide significantly faster, plasma-reduced GSH lower patients than diabetic PMNs showed no correlation with glucose concentrations, whereas a positive linear HbA lc found. than when each was incubated its own serum. vitro survival was reduced incubated serum, sera promoted PMNs. Peripheral counts higher in diabetic CONCLUSIONS Type is accompanied a priming of PMNs, resulting OS increased self-necrosis. Necrosis starts chain of inflammatory reactions that result recruitment long run, with OS, may endothelial dysfunction. Understanding contribution of inflammation illuminate new mechanisms through dysfunction evolves causes angiopathy and atherosclerosis.