椎间盘退变期间细胞自噬对MEK、ERK、NRF1、Atg7表达的影响

doi:10.3969/j.issn.1671-7171.2019.07.027

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Abstract 【Objective】To investigate the autophagy of mitogen-activated protein kinase (MEK), cell signal-regulated kinase (ERK), transcription factor CNC-bZIP protein (NRF1) and autophagy-associated protein 7 (Atg7) during intervertebral disc degeneration to explore the basic research and clinical treatment of lumbar degenerative changes. 【Methods】 A total of 18 patients with severe degeneration of lumbar intervertebral disc (Pfirrmann grade 5) in the observation group and 18 patients with young lumbar vertebrae fractures in the control group were selected as the study subjects. The nucleus pulposus cells were isolated from lumbar intervertebral disc tissue and CD24 positive cells were sorted by flow cytometry. The cells were cultured for 96 h under simulated physiological pressure. The expressions of MEK, ERK, NRF1 and Atg7 mRNA in nucleus pulposus cells were detected by RT-PCR. The levels of MEK, ERK, NRF1 and Atg7 protein in nucleus pulposus cells were detected by Western blot. 【Results】 Results of RT-PCR showed that the expression levels of MEK, ERK, NRF1 and Atg7 mRNA in the observation group were significantly higher than those in the control group t (P<0.05).Western blot results showed that the expression levels of MEK, ERK, NRF1 and Atg7 proteins in the observation group were higher than those in the control group. The differences between the two groups were statistically significant (P<0.05). 【Conclusion】Autophagy upregulates the expression of MEK, ERK, NRF1 and Atg7 proteins in nucleus pulposus cells during degeneration of intervertebral disc. The MEK/ERK/NRF1/Atg7 signaling pathway is the main signaling pathway regulating nucleus pulposus cell apoptosis and may be involved in the pathogenesis of lumbar degenerative changes.

Key words： Autophagy/PH Intervertebral Disc/CY

Received: 12 November 2018

PACS:

R329.25

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http://journal07.magtech.org.cn/yxlcyj/EN/10.3969/j.issn.1671-7171.2019.07.027 OR http://journal07.magtech.org.cn/yxlcyj/EN/Y2019/V36/I7/1326

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