导　　师： 周初松

学科专业： 100210

授予学位： 硕士

作　　者： ;

机构地区： 南方医科大学

摘　　要： Backgrounds Disc degeneration is the root cause of spinal anatomy and dysfunction disorder. Associated with spinal disc degeneration disease /(disc herniation, degenerative spinal stenosis, degenerative spondylolisthesis and spinal instability, degenerative scoliosis, etc/) increasing the incidence as the rhythm of life and society to speed up the aging process. Domestic and foreign scholars have got a certain understanding about its occurrence and development which addresses a relevant factor in disc degeneration, such as matrix metalloproteinase, protein polysaccharide enzymes, elastics, inflammatory mediators, cell factor; autoimmune response, nitrogen oxide and so on, but know little about the underlying causes of degeneration. In order to study the pathophysiology of disc degeneration mechanism, to explore the root causes of the occurrence and development, We applied proteomics methods in normal and degenerative intervertebral disc for two-dimensional electrophoresis and mass spectrometry,and discovered that the degeneration of nucleus pulposus in Peroxiredoxin II /(Prx II/) reductase exist in significant differential expression. But the role and its mechanism is unknown. Peroxiredoxins /(Prxs/) is a newly discovered molecular weight /(20-30/)×103 KD Peroxides family members, Prxs'function is diverse, including antioxidant, regulation of intracellular signal transduction involved in cell cycle progression and play a molecular chaperone and so on. Antioxidant role is the most important function H2O2 is one of the major substrates of Prxs, cells ues Prxs remove H2O2which is harmful to cells to achieve the purpose of protecting cells from damage. Recently years, however, H2O2 as second messenger signal transduction was paid more and more attention, and thus as an important regulator of Prxs has also become a research hotspot. Although previous studies have mostly focused on the Prxs on the protection of cells involved in cell signal transduction, cell differentiation, anti-oxidation, in recent year

关 键 词： 过氧化物酶 椎间盘 髓核细胞 型胶原 椎间盘退变

领　　域： [文化科学] [文化科学] [文化科学] [文化科学]