Swimming Inhibits Intervertebral Disc Degeneration via the Wnt/β-Catenin Pathway

Abstract

Objective: Intervertebral disc degeneration (IVDD) causes a variety of symptoms, including low back pain, herniated discs, and spinal stenosis, which impose high social and economic costs. We established a rat model of IVDD and then explored the effect of swimming exercise in IVDD rats. We aimed to investigate the role of the Wingless-Type mouse mammary tumor virus (MMTV) Integration Site Family (Wnt)/β-catenin pathway in this process. Methods: 45 three-month-old Sprague-Dawley (SD) rats were randomly divided into three groups: the Control group (267 ± 11 g), the Model group (260 ± 12 g), and the Model+Swimming group (262 ± 13 g). The Control group received no treatment; the Model group underwent surgery to establish an IVDD model; the rats in the Model+Swimming group received swimming training after the IVDD model was established. The intervertebral disc tissues of rats in each group were evaluated for degeneration using hematoxylin-eosin (H&E) staining, safranin O-fast green (SFG) staining, immunohistochemistry, real-time quantitative Polymerase Chain Reaction (RT-qPCR), and western blotting assays. The study assessed the effect of swimming training on IVDD and explored the expression of Wnt/β-catenin pathway-related proteins. Results: Based on H&E and SFG staining, the structure of intervertebral disc (IVD) was destroyed and the nucleus pulposus (NP) cells were lost in the Model group rats. However, swimming training could improve the damage to the IVD structure and loss of NP cells. Immunohistochemical results showed that the expressions of β-catenin and interleukin-1beta (Il-1β) in the IVD tissue of the Model group were higher than that in the Control group (p < 0.01). Conversely, the expressions of β-catenin and Il-1β in the IVD tissue of the Model+Swimming group were lower than that in the Model group (p < 0.01). RT-qPCR and western blot analyses showed that compared with the Control group, the expressions of Aggrecan and Collagen II proteins and messager RNAs (mRNAs) in the IVD of the Model group were down-regulated (p < 0.01), while the expressions of Il-1β, Wnt-1, and β-catenin proteins and mRNAs were up-regulated, which was statistically significant. Compared with the Model group, the expressions of Aggrecan and Collagen II in the IVD tissue of the Model+Swimming group were up-regulated, while the expressions of Wingless-type mouse mammary tumor virus (MMTV) integration site family member 1 (Wnt-1), β-catenin, and Il-1β were down-regulated. These findings indicated that swimming training could reduce the expression of inflammatory factors, improve the inflammation of degenerative IVDs in rats and promote the recovery of IVDD. Conclusions: Swimming training can improve the IVDD in rats and has positive application values.