Effect Of Transforming Growth Factor Beta (Tgf-Beta) On The Degeneration Of Intervertebral Discs By Regulating Nuclear Factor Kappa-Light-Chain-Enhancer Of Activated B Cells/Mammalian Target Of Rapamycin (Nf-Kappa B/Mtor) Signaling Pathway

Intervertebral disc degenerative disease (IDDD) is common in orthopedics. TGF-beta involves in inflammation and tissue repair. But its role in IDDD remains unclear. IDDD patients and normal intervertebral disc nucleus pulposus tissues were collected. IDDD was divided into prominent group and prolapse group. IDDD nucleus pulposus cells were isolated and divided into control group, TGF-beta agonist group and TGF-beta inhibitor group followed by analysis of cell proliferation by MTT, cell apoptosis by flow cytometry, BALP and OC expression by Real time PCR, NF-kappa B/mTOR signaling protein expression by Western blot as well as IL-1 and IL-6 secretion by ELISA. Compared with normal group, TGF-beta mRNA and serum level in patients with IDDD was significantly decreased (P < 0.05), with more significant changes in prolapse group (P < 0.01). Pfirrmann grading scores were negatively correlated with TGF-beta serum level (P < 0.001). TGF-beta agonists can significantly promote cell proliferation, inhibit apoptosis, upregulate BALP and OC expression, inhibit NF-kappa B expression, increased p-mTOR level and decrease IL-1 and IL-6 secretion (P < 0.05). All these changes were significantly reversed by TGF-beta inhibitors (P < 0.05). TGF-beta expression in IDDD is reduced and associated with disease severity. Promoting TGF-beta expression can inhibit inflammatory factors secretion, promote BALP and OC expression and cell proliferation, and inhibit the degeneration of intervertebral discs by regulating NF-kappa B/mTOR signaling.