Melatonin Inhibits Annulus Fibrosus Cell Senescence through Regulating the ROS/NF-κB Pathway in an Inflammatory Environment

Inflammation response is an important reason for disc cell senescence during disc degeneration. Recently, melatonin is suggested to protect against disc degeneration. However, the effects of melatonin on annulus fibrosus (AF) cell senescence are not fully studied. The main purpose of this study was to investigate the effects of melatonin on AF cell senescence in an inflammatory environment and the underlying mechanism. Rat disc AF cells were cultured in a medium with tumor necrosis factor-alpha (TNF-alpha). Melatonin was added along with the medium to observe its protective effects. Compared with the control AF cells, TNF-alpha significantly declined cell proliferation potency and telomerase activity, elevated senescence-associated beta-galactosidase (SA-beta-Gal) activity, upregulated protein expression of senescence markers (p16 and p53), and increased reactive oxygen species (ROS) content and activity of the NF-kappa B pathway. However, when the TNF-alpha-treated AF cells were incubated with melatonin, ROS content and activity of the NF-kappa B pathway were decreased, and those parameters reflecting cell senescence indicated that AF cell senescence was also partly alleviated. Together, melatonin suppresses AF cell senescence through regulating the ROS/NF-kappa B pathway in an inflammatory environment. This study sheds a new light that melatonin may be promising to retard inflammation-caused disc degeneration.