Glucosamine calmed IL-1 beta in human cartilage cells but did not change MMP13

What they did

Chondrocytes were isolated from femoral head cartilage of people having surgery for a fractured neck of femur, with ethical permission. They were cultured for five weeks in six groups: control; IL-1 beta plus oncostatin M (2.5 ng/ml each); 2 mM N-acetyl glucosamine; cytokines plus glucosamine; 1.0 µM BAY 11-7082, an NF-kB inhibitor; and cytokines plus BAY. The team measured IL1B and MMP13 messenger RNA, and the DNA methylation of each gene's promoter by pyrosequencing.

What they found

The cytokines raised IL1B expression more than 580-fold. Glucosamine reduced that by 4-fold. BAY alone raised IL1B 3-fold, but cut cytokine-induced IL1B by 6-fold. Methylation at one CpG site in the IL1B promoter fell from 65% in controls to 36% with cytokines, and glucosamine and BAY held it at 44% and 53%. The cytokines raised MMP13 mRNA whether or not glucosamine or BAY was present, and methylation of the MMP13 promoter did not change.

What it can't tell us

The cells came from hip fracture surgery rather than worn joints, and the abstract does not give the number of donors. The form tested was N-acetyl glucosamine at 2 mM in a dish, not glucosamine sulphate taken by mouth. It measured gene messages and methylation, not enzyme activity or cartilage tissue.

Why it matters

It is a useful counterweight. Other cell studies found glucosamine lowered MMP13, but here, under strong cytokine stimulation over five weeks, MMP13 rose regardless. A fair summary of glucosamine and MMP13 has to include results like this one alongside the positive ones.

The paper

1. Imagawa K, de Andrés MC, Hashimoto K et al. The epigenetic effect of glucosamine and a nuclear factor-kappa B (NF-kB) inhibitor on primary human chondrocytes--implications for osteoarthritis. Biochem Biophys Res Commun 2011.
   PMID 21219853DOI 10.1016/j.bbrc.2011.01.007

Read next