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Advanced Glycation End Products Induce Caudal Disc Degeneration in Ovariectomized Female Rats.

Xiao Liang1, Zhaohui Li2, Pengcheng Ren3

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JOR Spine
|September 11, 2025
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Summary

This study developed a reliable rat model for intervertebral disc degeneration (IVDD) using advanced glycation end products (AGEs) in ovariectomized rats. Results show AGEs induce dose-dependent IVDD, with estrogen offering a protective effect.

Keywords:
estrogenintervertebral disc degenerationrat advanced glycation end products

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Area of Science:

  • Biomedical research
  • Preclinical animal models
  • Degenerative diseases

Background:

  • Intervertebral disc degeneration (IVDD) necessitates reliable preclinical models for therapeutic development.
  • Advanced glycation end products (AGEs) are implicated in IVDD pathogenesis.
  • Ovariectomized rats provide a potential model for studying IVDD.

Purpose of the Study:

  • To establish a reproducible rat model of IVDD using AGE injections in ovariectomized rats.
  • To investigate the dose-dependent effects of AGEs on IVDD.
  • To explore the influence of endogenous estrogen on IVDD.

Main Methods:

  • Ovariectomized female Sprague-Dawley rats received AGE injections (0.5-4 μg) into coccygeal discs.
  • Control groups included needle puncture, vehicle injection, and non-ovariectomized rats.
  • IVDD was assessed via radiological, histological, and immunohistochemical analyses two weeks post-injection.

Main Results:

  • AGE injections successfully induced IVDD in a dose-dependent manner in ovariectomized rats.
  • No IVDD was observed in needle-puncture or vehicle-only control groups.
  • Non-ovariectomized rats exhibited less severe IVDD compared to ovariectomized counterparts, suggesting estrogen's protective role.

Conclusions:

  • A single AGE injection into caudal discs reliably induces IVDD in ovariectomized rats.
  • This model is suitable for studying IVDD mechanisms and testing therapies.
  • Endogenous estrogen demonstrates a protective effect against IVD degeneration.