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Updated: Oct 8, 2025

Operational and Intervention Effects of Targeted Tuina in Lumbar Intervertebral Disc Degeneration Model Rabbits
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A decrease in IL-33 regulates matrix degradation and apoptosis in intervertebral disc degeneration via HIF-1alpha.

Jinquan Hu1, Qiang Yan2, Hanran Jiang3

  • 1Department of Orthopedics, Changzheng Hospital Affiliated with Second Military Medical University 415 Fengyang Road, Shanghai 200003, China.

American Journal of Translational Research
|December 27, 2021
PubMed
Summary
This summary is machine-generated.

Interleukin-33 (IL-33) may treat intervertebral disc degeneration (IDD) by upregulating hypoxia-inducible factor-1alpha (HIF-1α), restoring extracellular matrix (ECM) and reducing low back pain (LBP).

Keywords:
ECMHIF-1αIL-33Low back painnucleus pulposus cells

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Area of Science:

  • Molecular Biology
  • Biochemistry
  • Regenerative Medicine

Background:

  • Low back pain (LBP) is often linked to intervertebral disc degeneration (IDD), characterized by extracellular matrix (ECM) imbalance.
  • Abnormal hypoxia-inducible factor-1alpha (HIF-1α) expression in nucleus pulposus (NP) cells is implicated in IDD pathogenesis.
  • The precise mechanisms reducing ECM in IDD remain incompletely understood.

Purpose of the Study:

  • To investigate the role of Interleukin-33 (IL-33) in the pathogenesis of intervertebral disc degeneration (IDD).
  • To explore the potential of IL-33 as a therapeutic target for IDD associated with low back pain (LBP).

Main Methods:

  • Assessed IL-33 and HIF-1α correlation in NP cells from individuals with IDD.
  • Overexpressed IL-33 in degenerative NP cells in vitro to evaluate its effects on ECM components (MMP-3/13, ADAMTS-4/5) and apoptosis markers (Caspase-3, Bcl-2).
  • Investigated the necessity of HIF-1α for IL-33's effects by silencing HIF-1α expression.

Main Results:

  • IL-33 levels were decreased and negatively correlated with HIF-1α in NP cells of IDD patients.
  • IL-33 overexpression reduced matrix-degrading enzymes (MMP-3/13, ADAMTS-4/5) and promoted ECM synthesis in vitro.
  • IL-33 exhibited anti-apoptotic effects by decreasing Caspase-3 and increasing Bcl-2 expression.
  • IL-33's ability to upregulate ECM was dependent on HIF-1α expression.

Conclusions:

  • IL-33 plays a protective role in intervertebral disc degeneration (IDD) by modulating ECM homeostasis and inhibiting apoptosis.
  • IL-33 upregulates ECM expression, at least partly, through the induction of HIF-1α.
  • Targeting the IL-33/HIF-1α pathway presents a promising therapeutic strategy for IDD and associated low back pain (LBP).