Berberine Prevents Human Nucleus Pulposus Cells From Il-1 Beta-Induced Extracellular Matrix Degradation And Apoptosis By Inhibiting The Nf-Kappa B Pathway

Intervertebral disc degeneration (IDD) is widely considered to be one of the main causes of lower back pain, which is a chronic progressive disease closely related to inflammation, nucleus pulposus (NP) cell apoptosis and extracellular matrix (ECM) degradation. Berberine (BBR) is an alkaloid compound with an anti-inflammatory effect and has been reported to exert therapeutic action in several inflammatory diseases, including osteoarthritis. Therefore, it was hypothesized that BBR may have a therapeutic effect on IDD through inhibition of the inflammatory response. The aim of the present study was to evaluate the influence of BBR on IDD in interleukin (IL)-1 beta-treated human NP cells in vitro. The results showed that BBR attenuated the upregulation of ECM-catabolic factors [matrix metalloproteinase (MMP)-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)-4 and ADAMTS-5], and the downregulation of ECM-anabolic factors (type II collagen and aggrecan) following stimulation of the human NP cells with IL-1 beta. Treatment with BBR also protected human NP cells from IL-1 beta-induced apoptosis, as determined by western blotting and flow cytometry. Mechanistically, the IL-1 beta-stimulated degradation of I kappa B alpha, and the phosphorylation and translocation of nuclear factor (NF)-kappa B p65 were found to be attenuated by BBR, indicating that NF-kappa B pathway activation was suppressed by BBR in the IL-1 beta-treated human NP cells. The results of the experiments revealed a therapeutic potential of BBR for the prevention or treatment of IDD.