Osteogenic protein-1 inhibits nucleus pulposus cell apoptosis through regulating the NF-?B/ROS pathway in an inflammation environment.

ABSTRACT:

Background

Intervertebral disc degeneration is a pathological process that involves an inflammation response. As a classical cellular feature, several studies have demonstrated that inflammation can promote nucleus pulposus (NP) cell apoptosis. Therefore, attenuation of NP cell apoptosis may be a potential way to retard disc degeneration.

Objective

The present study was aimed to investigate the protective effects of osteogenic protein-1 (OP-1) against NP cell apoptosis in an inflammation environment, and the potential signaling transduction pathway.

Methods

Rat NP cells were cultured in medium with or without inflammatory cytokine tumor necrosis factor (TNF)-? for 6 days. The exogenous TNF-? was added into the medium to investigate its protective effects. NP cell apoptosis was evaluated by cell apoptosis ratio, caspase-3 activity, gene/protein expression of apoptosis-related molecules (Bcl-2, Bax, and caspase-3). Additionally, the intracellular reactive oxygen species (ROS) content and activity of the NF-?B pathway were also analyzed.

Results

Compared with the control NP cells, TNF-? significantly increased cell apoptosis ratio, caspase-3 activity, gene/protein expression of Bcl-2, Bax and caspase-3, ROS content, and activity of the NF-?B pathway. However, OP-1 partly attenuated these effects in NP cells treated with TNF-?.

Conclusion

OP-1 is effective in attenuating TNF-?-caused NP cell apoptosis, and the ROS/NF-?B pathway may be the potential signaling transduction pathway. The present study indicates that OP-1 may be helpful to inhibit inflammation-mediated disc degeneration.

SUBMITTER: Yu W 

PROVIDER: S-EPMC6246766 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature