Rattima JeenapongsaKrongtong YoovathawornKittima M. SriwatanakulUbonwan PongprayoonKampon SriwatanakulNaresuan UniversityMahidol UniversityThailand Inst. of Sci./Technol. Res.2018-07-242018-07-242003-08-01Journal of Ethnopharmacology. Vol.87, No.2-3 (2003), 143-148037887412-s2.0-0038014031https://repository.li.mahidol.ac.th/handle/123456789/21028This study aimed to investigate the anti-inflammatory activity of (E)-1-(3,4-dimethoxyphenyl) butadiene (DMPBD), isolated from Zingiber cassumunar Roxb., using in vivo and in vitro models. The results show that DMPBD dose-dependently inhibited the rat ear edema induced by ethyl phenylpropiolate (EPP), arachidonic acid (AA) and 12-O-tetradecanoylphorbol 13-acetate (TPA) and it was more potent than any other standard drugs being used. In EPP-induced edema IC50of DMPBD and oxyphenbutazone were 21 and 136nmol per ear, respectively. The IC50of DMPBD and phenidone were 60 and 2520nmol per ear, respectively, in AA-induced edema whereas DMPBD was 11 times more potent than diclofenac in TPA-induced edema (IC50=660 and 7200pmol per ear, respectively). DMPBD and diclofenac inhibited the rat paw edema induced by carrageenan but not by platelet activating factor (PAF). In in vitro study DMPBD, aspirin and phenidone inhibited collagen-induced platelet aggregation with IC50of 0.35, 0.43 and 0.03mM, respectively. Whereas IC50of these agents in ADP, AA and PAF inductions were 4.85, 3.98 and 1.30mM; 0.94, 0.13 and 0.04mM; and 1.14, 6.96 and 2.40mM, respectively. These results indicate that DMPBD possesses a potent anti-inflammatory activity through the inhibition of CO and LO pathways and seems to have more prominent effects on the LO pathway. © 2003 Published by Elsevier Science Ireland Ltd.Mahidol UniversityPharmacology, Toxicology and PharmaceuticsArticleSCOPUS10.1016/S0378-8741(03)00098-9