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Related Experiment Video

Updated: Jun 6, 2025

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Curculigoside upregulates BMAL1 to decrease nucleus pulposus cell apoptosis by inhibiting the JAK/STAT3 pathway.

Linchuan Lei1, Hua Wang2, Zhuoyang Zhao1

  • 1Department of Spine Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, PR China; Guangdong Province Key Laboratory of Orthopedics and Traumatology, Guangzhou 510080, PR China; Laboratory of General Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, PR China.

Osteoarthritis and Cartilage
|December 2, 2024
PubMed
Summary

Curculigoside (CUR) alleviates intervertebral disc degeneration (IVDD) by upregulating BMAL1, reducing cell apoptosis and improving extracellular matrix. This offers a new therapeutic strategy for IVDD.

Keywords:
ApoptosisBMAL1CurculigosideIntervertebral disc degeneration

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Intervertebral disc degeneration (IVDD) is a common aging process and a primary cause of low back pain.
  • Basic helix-loop-helix ARNT-like 1 (BMAL1) is implicated in various disease pathologies.
  • Curculigoside (CUR) is investigated for its potential anti-apoptotic properties in disease contexts.

Purpose of the Study:

  • To investigate the role of BMAL1 in IVDD.
  • To explore the therapeutic potential of CUR in mitigating IVDD.
  • To elucidate the molecular mechanisms underlying CUR's effects on IVDD.

Main Methods:

  • RNA sequencing (RNA-seq) to identify dysregulated genes.
  • Western blotting (WB), immunohistochemistry, and immunofluorescence (IF) to assess BMAL1 expression.
  • Flow cytometry and cell-based assays to evaluate apoptosis and extracellular matrix (ECM) components in nucleus pulposus (NP) cells.
  • In vivo studies using BMAL1-knockout and IVDD mouse models, and therapeutic evaluation of CUR injection.

Main Results:

  • BMAL1 expression inversely correlated with IVDD severity, being lower in degenerative NP cells.
  • BMAL1 knockdown increased NP cell apoptosis, while overexpression reduced it.
  • CUR treatment upregulated BMAL1 by inhibiting STAT3 phosphorylation via the JAK-STAT3 pathway.
  • CUR treatment alleviated NP cell apoptosis and enhanced ECM production, thereby mitigating IVDD.

Conclusions:

  • CUR effectively inhibits apoptosis and enhances ECM production in IVDD by upregulating BMAL1.
  • This mechanism provides a novel therapeutic avenue for inflammation-induced IVDD.
  • The findings highlight CUR as a potential therapeutic agent for managing IVDD.