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

Background contextStudies 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.PurposeTo determine the effects of glucosamine HCl on pro-inflammatory mediator production by intervertebral disc cells.Study designAn in vitro, experimental study of interleukin-1 (IL-1) stimulated rat intervertebral disc cells treated with and without glucosamine HCl.MethodsRat 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-α), prostaglandin E2 (PGE2), and NO levels in the medium were quantified and compared across treatments.ResultsAnnulus cells, 7 days: Glucosamine completely inhibited IL-6 and TNF-α, increased NO (by 75%), and reduced viability (by 89%) compared with IL-1 alone. Nucleus cells, 7 days: Glucosamine reduced IL-6 (by 89%), PGE2 (91%), and NO (90%) with no effect to viability.ConclusionsGlucosamine 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.