Abstract
It is generally accepted that anti-inflammatory drugs (NSAID) act by inhibiting the synthesis of prostaglandin (PGs) . However, salicylic acid, the most ancient of these drugs, is an ineffective cyclooxygenase inhibitor, but is equipotent with aspirin in antiinflammatory activity, we have now investigated the effect of such salicylates as aspirin (ASA), salicylic acid (SA), methyl salicylate (MS) and glycol salicylate (GS) on experimental acute inflammation.
On rat paw edema induced by carrageenin, all salicylates showed the inhibitory effect in oral administration that was weak at 1 hr, but potent after 2 hrs. In local injection, all salicylates did not show the significant inhibition on paw edema, but in skin application as ointment, these drugs inhibited signi-ficantly the paw edema. The order of inhibitory activity on edema was ASA>SA≥MS≥GS. On guinea pig skin erythema induced by UV irradiation and arachidonic acid, all salicylates inhibited significantly only in early phase, but did not inhibit PGE2-induced erythema in all phase. The order of inhibitory activity on erythema was ASA>SA>GS≥MS.
This mode of action of salicylates was the same as that of general NSAID of cyclooxygenase inhibitors. Collagen- or arachidonic acid-induced aggregation of rat platelets and acute death of rabbits by arachidonic acid i.v. injection were inhibited by aspirin, whereas other three salicylates were inactive. A23187-, fMLP- and zymosan-induced active oxygen generation of rat leucocytes was not inhibited by all salicylates.
It may be suggested from these results that except a partial action of ASA, salicylates act as SA in viva and the anti-inflammatory activity of SA is due to inhibition of PGs production, and the mechanisms are not the inhibition of the platelets and leucocytes functions, but the unknown action.
