Journal of Clinical Medicine Research

Background: Disc degeneration usually results from inflammation, proliferation and apoptosis of nucleus pulposus cells, and is one of the main causes of low back pain. Controlling cell cycle protein B1 (CCNB1) delays the path of intervertebral disc degeneration.P53 controls the apoptosis of nucleus pulposus cells, which affects intervertebral disc degeneration. However, the exact link between P53 and CCNB1 in NP cells is not known at the moment. Objective: To study how interactions between CCNB1 and P53 impact nucleus pulposus cells apoptosis in the mechanism of intervertebral disc degeneration. Methods: Nucleus pulposus tissue from patients with lumbar spine surgery was collected for analysis. Expression of p53, CCNB1, Bax, caspase-3, BCL-2, and COL2A1 was measured by qRT-PCR and Western Blot techniques. TNF-α was used to induce degeneration of isolated nucleus pulposus cells, cultured and transfected with siRNA-P53. Cell viability, proliferation and apoptosis were measured by CCK-8 and flow cytometry, respectively. Results: Degenerated nucleus pulposus tissues from intervertebral discs exhibited elevated levels of p53, Bax, and caspase-3, alongside decreased levels of CCNB1, BCL-2, and COL2A1. Silencing p53 in these cells resulted in increased expression of CCNB1, BCL-2, and COL2A1, while decreasing levels of p53, Bax, and caspase-3. This intervention enhanced cell viability and proliferation, while reducing apoptosis. Conclusion: These findings suggest that silencing p53 may upregulate CCNB1 expression, thereby inhibiting apoptosis in NP cells and potentially delaying the degeneration of intervertebral discs.