Galangin Alleviates Intervertebral Disc Degeneration via the Nrf2/NF-κB Pathway

In the pathogenesis of intervertebral disc diseases, the degeneration of nucleus pulposus cells (NPCs) stands as a pivotal factor. Galangin (GAL), a type of natural flavonoid, boasts various bioactivities, including Anti-aging and antioxidation. However, its effects on NPCs and the underlying mechanisms have not been fully elucidated. This study is devoted to probing into the impact of GAL on NPC degeneration along with the potential molecular pathways involved. IL-1β was utilized to replicate the pathophysiological conditions typical of intervertebral disc degeneration (IVDD). In NPCs treated with IL-1β, it was revealed that GAL not only markedly diminished the levels of pro-inflammatory factors and curbed the degradation of the extracellular matrix (ECM) but also modulated the NF-κB signaling pathway. From a mechanistic perspective, GAL realized these effects by activating nuclear factor erythroid 2-related factor 2 (Nrf2) and restraining its ubiquitination, which in turn led to the downregulation of NF-κB. Moreover, in in vivo studies employing rat models of puncture-induced IVDD, GAL demonstrated significant therapeutic efficacy, especially in hindering the progression of IVDD. This study highlights that GAL holds great promise for slowing the progression of IVDD by regulating the Nrf2/NF-κB pathway, casting GAL as a prospective and cutting-edge therapeutic target for IVDD.

NF-κB pathway; Nrf2; galangin; inflammation; intervertebral disc degeneration.