氧化应激诱导椎间盘细胞衰老研究进展

椎间盘细胞衰老是随着年龄的增加以及外界多种因素的刺激，椎间盘内的活性氧不断蓄积，椎间盘细胞的氧化应激状态从而被激活引起的。虽然目前仍然不能够明确氧化应激引起椎间盘细胞衰老的具体机制，但对近年来国内外有关细胞衰老机制的相关文献研究，为本研究提供帮助。本研究推测氧化应激也是通过DDR通路、核因子KB通路、p38MAPKs通路和microRNA通路四种方式来诱导椎间盘细胞衰老，分别作用于p16……途径或p19“。／p53／p21途径，对下游靶基因进行调控，从而抑制细胞增值导致细胞老化。但其主要作用方式尚不明确，主要作用途径及作用靶点仍有待验证，这是寻找特异性强、安全、高效的药物来防治椎间盘退变性疾病的前提条件。

Reseach Progress of Oxidative Stress Inducing Intervertebrai Disc Cell Aging

With the increase of age, and the stimulation of the various external factors, the constant accumulation of active oxygen inside the disc, and oxidative stress state can be activated ,which leaded to intervertebral disc cell aging. Although it still can＇t clarify the specific mechanism of oxidative stress causing intervertebral disc cells aging, related literatures researches on cell aging mechanism at home and abroad provide plenty of help for this study. This study speculates that oxidative stress also induces intervertebral disc cell aging through four ways of DDR pathway, nuclear factor kappa B pathway, p38 MAPKs pathway and microRNA pathways, and respectively act on pl6INK4a way or p19ARF/p53/p21 way, regulation of the downstream target genes, thus inhibition of cell proliferation leading to cell aging. But its main action way is not clear, and the main pathways and targets remains to be verified, which are the precondition for findingstrong specificity, safe and effective drugs to prevention and treatment of degenerative disc disease.