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

Abstract

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. To determine the effects of glucosamine HCl on pro-inflammatory mediator production by intervertebral disc cells. An in vitro, experimental study of interleukin-1 (IL-1) stimulated rat intervertebral disc cells treated with and without glucosamine HCl. 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. 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. 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.