Glucosamine HCl alters production of inflammatory mediators by rat intervertebral disc cells in vitro

Spine J. 2007 Sep-Oct;7(5):601-8. doi: 10.1016/j.spinee.2006.10.012. Epub 2007 Jan 2.

Abstract

Background context: Studies on cartilage have shown anti-inflammatory effects of glucosamine related to inhibition of inflammatory mediators. Intradiscal injection of glucosamine has been proposed as a treatment for chronic discogenic low back pain. However, there have been no studies of the direct effects of glucosamine on disc cells.

Purpose: To determine the effects of glucosamine HCl on pro-inflammatory mediator production by intervertebral disc cells.

Study design: An in vitro, experimental study of interleukin-1 (IL-1) stimulated rat intervertebral disc cells treated with and without glucosamine HCl.

Methods: Rat annulus and nucleus cells were cultured in alginate beads and exposed to IL-1a (10 ng/mL)+glucosamine HCl (4.5 mg/mL), IL-1 alone, or neither for 4 and 7 days. Cell viability and IL-6, tumor necrosis factor alpha (TNF-alpha), prostaglandin E(2) (PGE(2)), and NO levels in the medium were quantified and compared across treatments.

Results: Annulus cells, 7 days: Glucosamine completely inhibited IL-6 and TNF-alpha, increased NO (by 75%), and reduced viability (by 89%) compared with IL-1 alone. Nucleus cells, 7 days: Glucosamine reduced IL-6 (by 89%), PGE(2) (91%), and NO (90%) with no effect to viability.

Conclusions: Glucosamine inhibits inflammatory mediator production by IL-1 stimulated disc cells, but also adversely affects the viability of rat annulus cells. The response is cell-type dependent, illustrated by differences for annulus and nucleus cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Survival / drug effects
  • Cells, Cultured
  • Dinoprostone / metabolism
  • Extracellular Matrix / immunology
  • Extracellular Matrix / metabolism
  • Glucosamine / pharmacology*
  • In Vitro Techniques
  • Inflammation Mediators / metabolism*
  • Interleukin-1alpha / pharmacology
  • Interleukin-6 / metabolism
  • Intervertebral Disc / cytology*
  • Intervertebral Disc / drug effects*
  • Intervertebral Disc / immunology
  • Male
  • Nitric Oxide / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Inflammation Mediators
  • Interleukin-1alpha
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Dinoprostone
  • Glucosamine