作者: Stefanie Dimmeler , Susanne Brinkmann , Edmund Neugebauer
DOI: 10.1016/0014-2999(95)00499-8
关键词: Methylprednisolone 、 Glucocorticoid 、 Lipopolysaccharide 、 Endothelial stem cell 、 Internal medicine 、 Oxidative stress 、 Cytotoxic T cell 、 Aminosteroid 、 Biology 、 Permeability (electromagnetism) 、 Endocrinology
摘要: Endotoxic shock results in endothelial cell dysfunction and oedema formation. Endotoxin decreased a concentration-dependent fashion viability with maximum effects by adding 10 μg/ml lipopolysaccharide for 48 h (47 ± 15% 22 2.6% of control cells the presence or absence foetal calf serum, respectively). Furthermore, incubation (10 h) lower concentrations (1 μg/ml) significantly increased permeability to 250% compared values. The 21-aminosteroid U-74389G μM) prevented cytotoxic effect as well lipopolysaccharide-induced increase permeability. By contrast, glucocorticoid methylprednisolone was less effective even at higher (100 μM). is possibly due oxidative stress and/or membrane destabilization rather than induction inflammatory mediators, because reduced efficacy glucocorticoid.