Baicalin alleviates intervertebral disc degeneration by inhibiting the p38 MAPK signaling pathway

  • Exp Gerontol. 2025 Jun 1:204:112743. doi: 10.1016/j.exger.2025.112743.
Yating Wu  1 ,  Fengrui Li  1 ,  Shibin Shu  2 ,  Zhenhua Feng  2 ,  Yong Qiu  2 ,  Sen Li  2 ,  Zezhang Zhu  3
Affiliations
  • 1. Division of Spine Surgery, Department of Orthopedic Surgery, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, China.
  • 2. Division of Spine Surgery, Department of Orthopedic Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
  • 3. Division of Spine Surgery, Department of Orthopedic Surgery, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, China; Division of Spine Surgery, Department of Orthopedic Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China. Electronic address: [email protected].
PMID: 40174870 DOI: 10.1016/j.exger.2025.112743
Abstract

Background: Intervertebral disc degeneration (IVDD) represents a prevalent degenerative pathology of the spinal, primarily precipitated by inflammatory processes and the deterioration of extracellular matrix (ECM). Baicalin has an effective anti-inflammatory effect on degenerative diseases. In addition, the P38 mitogen-activated protein kinase (MAPK) signaling pathway plays a crucial role in the pathogenesis of IVDD.

Objective: To investigate the therapeutic potential of baicalin in modulating pathological changes in IVDD.

Methods: To design an in vitro model of degeneration of nucleus pulposus cells (NPCs) stimulated by IL-1β and an in vivo mouse model of needling to assess the protective effect of baicalin against IVDD and its underlying mechanism.

Results: Baicalin down-regulated inflammatory factors (iNOS, COX-2, IL-6) and catabolic factors (MMP-3, MMP-13, ADAMTS-5) while up-regulating anabolic factors (Collagen II, SOX-9) by inhibiting the activation of the p38 MAPK signaling pathway, in addition to slowing down the progression of IVDD in the mouse acupuncture model.

Conclusion: Our study demonstrated in vitro experiments that baicalin attenuates IL-1β-stimulated IVDD by inhibiting activation of the p38 MAPK signaling pathway. Meanwhile, the effects of baicalin were also confirmed in vivo experiments, Consequently, we propose that baicalin is a promising therapeutic agent for the treatment of disc degeneration.

Keywords
Baicalin; Extracellular matrix; Inflammation; Intervertebral disc degeneration; Nucleus pulposus cells.
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