SIRT3 retards intervertebral disc degeneration by anti- oxidative stress by activating the SIRT3/FOXO3/SOD2 signaling pathway

被引:41
作者
Zhou, T. -Y. [1 ]
Wu, Y. -G. [2 ]
Zhang, Y. -Z. [3 ]
Bao, Y. -W. [4 ]
Zhao, Y. [5 ]
机构
[1] Inner Mongolia Univ Nationalities, Affiliated Hosp, Dept Western Med Orthopaed, Tongliao, Peoples R China
[2] Bayannur Hosp, Dept Joint Surg, Bayannur, Peoples R China
[3] Inner Mongolia Univ Nationalities, Affiliated Hosp, Dept Orthopaed, Tongliao, Peoples R China
[4] Inner Mongolia Univ Nationalities, Affiliated Hosp, Operating Room, Tongliao, Peoples R China
[5] Inner Mongolia Med Univ, Affiliated Hosp 2, Dept Thoracolumbar Spine Surg, Hohhot, Peoples R China
基金
中国国家自然科学基金;
关键词
Intervertebral disc degeneration; SIRT3; Oxidative stress; SIRT3-DEPENDENT DEACETYLATION; CELL-DEATH; FIBROSIS;
D O I
10.26355/eurrev_201911_19408
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
OBJECTIVE: The objective of this paper is to determine whether SIRT3 could retard intervertebral disc degeneration and study the mechanism. MATERIALS AND METHODS: We chose the 3-month mice to establish intervertebral disc degeneration model and study the effect of SIRT3 on the intervertebral disc by Western blotting, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), immunohistochemistry. Mouse nucleus pulposus cells were cultured to study the exact mechanism. RESULTS: The expression of SIRT3 was decreased in degenerated human nucleus pulposus. Intervertebral discs of mice treated with theacrine expressed more collagen II and less collagen X. In addition, nucleus pulposus cells stimulated with interleukin-1 beta (IL-1 beta) expressed less SIRT3 than that in the control group and nucleus pulposus cells with SIRT3 overexpress vectors expressed more collagen II FOXO3a and superoxide dismutase 2 (SOD2), indicating that SIRT3 could improve the intervertebral disc degeneration by anti-oxidative stress. CONCLUSIONS: SIRT3 is a protective factor for intervertebral discs and can reduce oxidative stress in the intervertebral disc.
引用
收藏
页码:9180 / 9188
页数:9
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