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Life Sci. 2018 Apr 15;199:122-130. doi: 10.1016/j.lfs.2018.03.020. Epub 2018 Mar 9.

Melatonin resists oxidative stress-induced apoptosis in nucleus pulposus cells.

Author information

1
Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
2
Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address: cm95588@hust.edu.cn.
3
Department of Medical Ultrasound, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
4
Department of Orthopaedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
5
Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address: szwpro@163.com.

Abstract

AIMS:

Intervertebral disc degeneration (IVDD) is thought to be the major cause of low back pain (LBP), which is still in lack of effective etiological treatment. Oxidative stress has been demonstrated to participate in the impairment of nucleus pulposus cells (NPCs). As the most important neuroendocrine hormone in biological clock regulation, melatonin (MLT) is also featured by good antioxidant effect. In this study, we investigated the effect and mechanisms of melatonin on oxidative stress-induced damage in rat NPCs.

MAIN METHODS:

Cytotoxicity of H2O2 and protecting effect of melatonin were analyzed with Cell Counting kit-8 (CCK-8). Cell apoptosis rate was detected by Annexin V-FITC/PI staining. DCFH-DA probe was used for the reactive oxygen species (ROS) detection. The mitochondrial membrane potential (MMP) changes were analyzed with JC-1 probe. Intracellular oxidation product and reductants were measured through enzymatic reactions. Extracellular matrix (ECM) and apoptosis associated proteins were analyzed with Western blot assays.

KEY FINDINGS:

Melatonin preserved cell viability of NPCs under oxidative stress. The apoptosis rate, ROS level and malonaldehyde (MDA) declined with melatonin. MLT/H2O2 group showed higher activities of GSH and SOD. The fall of MMP receded and the expression of ECM protein increased with treatment of melatonin. The mitochondrial pathway of apoptosis was inhibited by melatonin.

SIGNIFICANCE:

Melatonin alleviated the oxidative stress-induced apoptosis of NPCs. Melatonin could be a promising alternative in treatment of IVDD.

KEYWORDS:

Apoptosis; Intervertebral disc degeneration; Melatonin; Nucleus pulposus cells; Oxidative stress

PMID:
29526797
DOI:
10.1016/j.lfs.2018.03.020
[Indexed for MEDLINE]

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