The mTOR pathway is involved in the process of platelet-rich plasma improving intervertebral disc degeneration.

Abstract

Objectives: Platelet-rich plasma (PRP) contains multiple growth hormones that may stimulate tissue repair. We aimed to assess PRP's efficacy and explore possible mechanisms using the intervertebral disc degeneration (IDD) model.

Materials and methods: A total of 48 male Sprague-Dawley (SD) rats were randomly divided into three groups: sham, IDD+PBS, and IDD+PRP (n=16, respectively). IL-1β (10 ng/ml) was used to establish a humanized IDD model in human lumbar nucleus pulposus (NP) tissues from 36 patients with degenerative disc disease. These NP cells were randomly divided into three groups: sham, IDD+PBS, and IDD+PRP (n=12, respectively). RT-PCR and western blot were used to detect the expression of aggrecan, collagen II, IL-1β, IL-6, TNF-α, Bcl-2, cleaved-Caspase 3, Bax and Akt/mTOR/p70S6K signaling pathway. A related assay kit was used to detect MDA, SOD, and GSH.

Results: PRP affected the expression of aggrecan, collagen II, IL-1β, IL-6, TNF-α, MDA, SOD, GSH, Bcl-2, cleaved-Caspase 3, and Bax in IDD rats. Compared with the IDD+PBS group, the expression of p-mTOR, p-p70/S6K, and p-Akt was much lower in the rat IDD+PRP group (P<0.05). Similarly, with PRP treatment in the humanized IDD model, the expression of p-mTOR, p-p70/S6K, and p-Akt was also inhibited.

Conclusion: PRP may be a potential therapy for IDD via the mTOR signaling pathway in regulating and affecting extracellular matrix degradation, inflammatory factors, oxidative stress, and apoptosis.