Related Experiment Video
Updated: Mar 9, 2026
Operational and Intervention Effects of Targeted Tuina in Lumbar Intervertebral Disc Degeneration Model Rabbits
Published on: July 21, 2023
Albiflorin Relieves Intervertebral Disc Degeneration Through Inhibiting Nucleus Pulposus Cell via the p38 MAPK/NF-κB
Kai Yang1, Yanping Cheng1, Dan Yang2
1Department of Rehabilitation Medical, Yangtze River Shipping General Hospital, Wuhan, Hubei Province, China.
Background:
As a chronic musculoskeletal disorder, intervertebral disc degeneration (IDD) is a leading cause of low back pain. Inflammatory response plays a key role in the IDD progression. Albiflorin (AF), a bioactive compound derived from Paeonia lactiflora, exhibits anti-inflammatory effects in various diseases. However, the effects of AF on IDD remain unexplored. This study explored the protective effect of AF against IDD and elucidate its possible mechanisms.
Methods:
Nucleus pulposus (NP) cells were stimulated with lipopolysaccharide (LPS ) for 24 h to establish the IDD cell model, followed by AF or p38MAPK agonist (P79350) treatment. Cell viability and apoptosis were evaluated using 5-ethynyl-2'-deoxyuridine (EdU) assay and flow cytometry analysis, respectively. Levels of the Inflammatory cytokines (tumor necrosis factor alpha, TNF-α; interleukin-1beta, IL-1β; IL-6) were assessed by enzyme-linked immunosorbent assay (ELISA). The mRNA levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-Associated X (Bax), aggrecan, and collagen type II was analyzed by reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR), while their protein levels were determined by western blot assay.
Results:
LPS induction remarkably inhibited NP cell proliferation (p < 0.001) and induced apoptosis (p < 0.001), which were significantly reversed by AF dose-dependently. Furthermore, AF treatment dose-dependently decreased extracellular matrix (ECM) degradation and inflammatory factors secretion in LPS-induced NP cells, evidenced by enhanced aggrecan and collagen type II protein expression (all p < 0.01), and reduced TNF-α, IL-1β, and IL-6 section (all p < 0.05). Mechanistically, AF exerted its protective effects by suppressing the p38 mitogen-activated protein kinase (MAPK)/nuclear factor κB (NF-κB) signaling pathway, as evidenced by reduced phosphorylation of p38 and p65 (all p < 0.01). Notably, co-treatment with P79350 partially abolished the protective effects of AF against LPS-induced NP cell damage.
Conclusion:
AF relieved IDD through repressing NP cell apoptosis, inflammatory response, and ECM degradation through the p38 MAPK/NF-κB pathway, indicating that it is a potential IDD therapeutic agent.
