Prostaglandin biosynthesis is not affected by the anti-inflammatory effect of turpentine.
In turpentine-pretreated rats, the development of carrageenan induced oedema is reduced, while dextran and PGE2-induced oedemas are not influenced. In these pretreated rats, carrageenan oedema is potentiated by arachidonic acid, the hypotensive effect of arachidonic acid is not decreased and the production of malonaldehyde by platelets is not inhibited. Thus, the reduction of carrageenan oedema in turpentine treated-rats does not appear to depend on an endogenous PG synthesis inhibition, while plasma level of acute phase reactants is greatly increased.
D000818:Animals; D000893:Anti-Inflammatory Agents; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D001798:Blood Proteins / Q000378:metabolism; D002351:Carrageenan; D015232:Dinoprostone; D004487:Edema / Q000139:chemically induced; D008315:Malondialdehyde / Q000097:blood; D011453:Prostaglandins / Q000096:biosynthesis*; D011458:Prostaglandins E / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D014425:Turpentine / Q000633:toxicity*
D000893:Anti-Inflammatory Agents; D001095:Arachidonic Acids; D001798:Blood Proteins; D011453:Prostaglandins; D011458:Prostaglandins E; D016718:Arachidonic Acid; D008315:Malondialdehyde; D002351:Carrageenan; D015232:Dinoprostone; D014425:Turpentine