Melatonin protects vertebral endplate chondrocytes against apoptosis and calcification via the Sirt1‐autophagy pathway

• DOI: 10.1111/jcmm.13903
• Publication Date: 2018-10-24T10:11:49Z
• Authors: Zengjie Zhang; Jialiang Lin; Naifeng Tian; Yaosen Wu; Yifei Zhou; Chenggui Wang; Qingqing Wang; Haiming Jin; Tingting Chen; Majid Nisar; Gang Zheng; Tianzhen Xu; Weiyang Gao; Xiaolei Zhang; Xiangyang Wang
• Keywords: Male; 0301 basic medicine; 0303 health sciences; Carbazoles; Calcinosis; Apoptosis; Original Articles; Intervertebral Disc Degeneration; Protective Agents; Rats, Sprague-Dawley; Disease Models, Animal; Oxidative Stress; 03 medical and health sciences; Chondrocytes; Sirtuin 1; tert-Butylhydroperoxide; Autophagy; Animals; Female; Cells, Cultured; Melatonin

Melatonin is reportedly associated with intervertebral disc degeneration (IDD). Endplate cartilage vitally important to discs in physiological and pathological conditions. However, the effects mechanism of melatonin on endplate chondrocytes (EPCs) are still unclear. Herein, we studied EPC apoptosis calcification elucidated underlying mechanism. Our study revealed that treatment decreases incidence inhibits a dose-dependent manner. We also found upregulates Sirt1 expression activity promotes autophagy EPCs. Autophagy inhibition by 3-methyladenine reversed protective effect calcification, while inhibitor EX-527 suppressed melatonin-induced against indicating beneficial EPCs mediated through Sirt1-autophagy pathway. Furthermore, may ameliorate IDD vivo rats. Collectively, this reduces be related pathway regulation, which help us better understand association between IDD.