British Journal of Rheumatology 1997;37:27-31
Abstract reprinted with permission of publisher
Oxford University Press ©1997

S. GUTIERREZ, I. PALACIOS, O. SANCHEZ-PERNAUTE, P, HERNANDEZ, J. MORENO, J. EGIDO and G. HERRERO-BEAUMONT

S-Adenosyl-L-methionine (SAMe) is a naturally occurring compound involved in transmethylation and trans-sulphuration reactions. The administration of SAMe to patients with osteoarthritis (OA) seems to have a protective effect, although the mechanisms of its action are largely unknown. We have studied the effect of SAMe as a protective agent against the modifications induced by tumour necrosis factor alpha (TNFa) on synovial cell proliferation and extracellular matrix protein synthesis, two important hallmarks of progressive articular diseases. The stimulation of cells with 100 U/ml TNFa (for 24 h decreased the proliferative rate (58"14% with TNFa vs basal 100%, P < 0.05), fibronectin (FN) mRNA expression (36" 14% vs basal, P < 0.05) and FN synthesis (79" 20% vs basal, P > 0.05). By contrast, TNFa raised total protein and proteoglycan synthesis (127 " 12% vs basal and 239 " 40% vs basal, respectively, P < 0.05). The addition of increasing concentrations of SAMe (10^-10-10^-6M) to synoviocytes incubated with TNFa reversed the effects induced by the cytokine, while SAMe alone did not modify significantly the metabolic processes studied. These results indicate that, in cultured synovial cells, SAMe restores basal conditions after cell damage elicited by TNFa stimulation.