Notably, co-treatment with P79350 partially abolished the protective effects of AF against LPS-induced NP cell damage.<h4>Conclusion</h4>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. Here, NFKB1 is linked to atrial fibrillation.