Study: Effects of SAMe | Equine Clinical Research
British Journal of Rheumatology 1997;37:27-31
Abstract reprinted with permission of publisher
Oxford University Press ©1997
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.
Abstract reprinted with permission of publisher
Oxford University Press ©1997
SAMe RESTORES THE CHANGES IN THE PROLIFERATION AND IN THE SYNTHESIS OF FIBRONECTIN AND PROTEOGLYCANS INDUCED BY TUMOUR NECROSIS FACTOR ALPHA ON CULTURED RABBIT SYNOVIAL CELLS
S. GUTIERREZ, I. PALACIOS, O. SANCHEZ-PERNAUTE, P, HERNANDEZ, J. MORENO, J. EGIDO and G. HERRERO-BEAUMONT
SUMMARY
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.
