Abstract
Introduction
Animal model was used to study the effects of chronic unpredictable stress (CUS) on the intervertebral disk (IVD). Stress is a predictor for low back disability in persons with earlier low back pain (LBP) and LBP is most common in the early stages of IVD degeneration. Stress can increase proinflammatory cytokines. Elevated levels of molecular mediators of inflammation have been described in the pathology of IVD degeneration; however, the effect of chronic stress on the induction of disk degeneration has not yet been clarified.
Materials and Methods
Cellular events involved in injury-and stress-induced disk degeneration in male Wistar rats were investigated. Disk degeneration and apoptosis was evaluated by microscopic (light and electron) and molecular (immunoblotting and immunohistochemistry) methods. Corticosterone levels were measured by radioimmunoassay as a marker of stress condition.
Results
The data showed that chronic stress could significantly increase corticosterone levels. Furthermore, biochemical markers of apoptosis (increased Bax to Bcl2 ratio (p < 0.05) and TUNEL reactivity) were observed in animals that had chronic stress. Electron and light microscopy also showed disk degeneration and apoptotic cells in over experimental group.
Conclusion
Taken together, the data demonstrated that chronic stress is probably a risk factor for creating IVD degeneration and that programmed cell death is one of the mechanisms of stress-induced disk degeneration, however, the effects of stress and its impact on the escalation of disk degeneration and LBP need to be clarified by further investigations.
Yes
None declared