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Low back pain caused by intervertebral disc degeneration (IVDD), a common orthopedic disease in middle-aged and elderly populations, burdens patients’ quality of life and work capacity. IVDD is closely associated with nucleus pulposus cell apoptosis and autophagy, mediated by BCL2, CASP3, CASP8, and CASP9. Although Duhuo alleviates inflammation and delays IVDD, its molecular mechanism remains unclear. We used bioinformatics to identify IVDD-related apoptotic/autophagic pathways and Duhuo’s therapeutic mechanisms via network pharmacology. Bioinformatic analysis showed high expression of NLRP3, IL6, AKT1, and MMP9 in IVDD patients, with key cellular processes including senescence, apoptosis, autophagy, and ferroptosis, critical signaling pathways (HIF-1, FoxO, and PI3K-Akt), and main immune cells (T cells and Th17 cells). Network pharmacology identified Duhuo’s main active components (ammidin, isoimperatorin, β-sitosterol, O-acetylcolumbianetin, and angelol D) and 23 potential targets, among which BCL2, CASP3, CASP8, CASP9, ERR1, and PTGS1 are crucial. Enrichment analysis indicated Duhuo prevents IVDD by regulating apoptosis, autophagy, HIF-1, and PI3K-Akt pathways, and molecular docking confirmed β-sitosterol effectively binds key targets. This study identifies IVDD’s molecular basis and establishes a mechanism for targeted regulation of nucleus pulposus cell apoptosis/autophagy to prevent IVDD progression.
Yan et al. (Fri,) studied this question.