论文部分内容阅读
TNF-α是极为重要的促炎性细胞因子, 在调节细胞免疫反应中起着多种生理和病理作用. TNF- α能激活血管内皮细胞, 继而表达多种细胞因子和黏附分子引发一系列的炎性白细胞浸润和炎症反应. 研究发现TNF-α炎性刺激除了能引起内皮细胞死亡外, 还能诱导内皮细胞的衰老. TNF-α处理的血管内皮细胞衰老相关的β-半乳糖苷酶染色反应显示阳性, 细胞周期停滞在G0~G1期; 内皮细胞中线粒体膜电位早期上升, 衰老时则降低, 表征早期细胞线粒体功能亢进, 而后期功能衰退; 活性氧水平早期有上升和下降的振荡, 诱导衰老后有所降低. 结果表明线粒体的功能变化与TNF-α诱导的内皮细胞衰老 有关.
TNF-α is a very important proinflammatory cytokine that plays a variety of physiological and pathological roles in the regulation of cellular immune response.NF-α activates vascular endothelial cells, which in turn express a variety of cytokines and adhesion molecules that trigger a series of Inflammatory leukocyte infiltration and inflammatory reaction.Studies found that TNF-αinflammatory stimuli can not only induce endothelial cell death, but also induce the senescence of endothelial cells.Serum TNF-α-treated vascular endothelial cell senescence-relatedβ-galactosidase staining The reaction was positive, the cell cycle arrest in the G0 ~ G1 phase; endothelial cell mitochondrial membrane potential increased early, decreased senescence, indicating early mitochondrial function hyperthyroidism, and late decline; reactive oxygen species rise and fall early oscillation, The results showed that the functional changes of mitochondria were related to the senescence of endothelial cells induced by TNF-α.