Integrated Bioinformatics and Molecular Docking Analysis Reveals Potential Mechanisms of Coptidis Rhizoma in Intervertebral Disc Degeneration

Abstract

Intervertebral disc degeneration (IVDD) is a major contributor to chronic low back pain and involves extracellular matrix degradation, inflammation, oxidative stress, and immune cell infiltration. This study integrated transcriptomic analysis, network pharmacology, molecular docking, molecular dynamics (MD) simulation, and ADMET prediction to explore potential mechanisms of Coptidis rhizoma (CR) in IVDD. Bioactive CR compounds and predicted targets were identified from TCMSP, SwissADME, and SwissTargetPrediction, and IVDD-related differentially expressed genes were obtained from two GEO datasets after normalization and batch-effect correction. Thirty-six overlapping genes were identified, and network analysis prioritized CCR1, CXCR2, ICAM1, TNF, STAT3, MPO, and MMP9 as core targets. Enrichment analyses highlighted chemokine signaling, cytokine–cytokine receptor interaction, leukocyte transendothelial migration, TNF signaling, IL-17 signaling, and NF-κB signaling. Docking and benchmark analyses indicated favorable predicted binding of Obacunone–CCR1 and Quercetin–MMP9, while 100-ns MD simulation supported the stability of the Obacunone–CCR1 complex. These findings suggest that CR may modulate chemokine-driven immune recruitment and downstream inflammatory-catabolic processes in IVDD, providing a hypothesis-generating basis for experimental validation.