Estudo farmacológico do óleo essencial dealpinia Zerumbet (PERS) B. L. BURT et R. M. e seus principais constituintes químicos, 4-TERPINEOL E 1,8-CINEOL, em músculo liso respiratório de rato

Abstract

Alpinia zerumbet (Pers) B. L. Burt. et R. M., popularly called “colônia” in Brazilian Northeastem, is an aromatic plant of the Zingiberaceae family that is used in folk medicine all over the world. Thus, this study aimed to characterize the pharmacological effects of the essential oil of Alpinia zerumbet (EOAz) and its two major Chemical constituents, 4-terpineole (TERP) and 1,8-cineole (CIN) on mouse respiratory smooth muscle. Tracheal rings were mounted in a superfusion chamber for isolated ex vivo muscle. EOAz, TERP and CIN at 1-1000 pg/mL did not affetc basal tone except for EOAz (100 pg/mL) and CIN (600 pg/mL) that induzed a small contraction. EOAz (1-1000 pg/mL) blocked with similar potency the contraction induced by acetylcholine (ACh; 30 pM), prostaglandin F2a (PGF2a; 30 pM), 5- hydroxytriptamine (5-HT; 10 pM), and 60 mM K+ (ICso= 280.76 pg/mL, 194.73 pg/mL, 315.05 pg/mL, and 162.56 pg/mL, respectively). EOAz relaxed pre-contracted preparations that were maintained in presence of PGF2a, 5-HT, and K+. Furthermore, EOAz relaxed preparations previously submitted to epinephrine. EOAz-induced muscle relaxation was not altered by the presence of lco-nitro-L-arginine methyl ester hydrochloride (L-NAME; 500 pM), cafeine (1 mM), and indomethacin (2 pM). EOAz (600 pg/mL) blocked the contractions induced by ACh (60 pM) in nutrient Solutions with nifedipine (10 pM) or in zero Ca2+ solution. EOAz (1000 pg/mL) fully blocked Ca2+-induced contractions in solution with 80 mM K+ in the presence of cafeine (5 mM). TERP (1-1000 pg/mL) blocked ACh and PGF2a-induced contractions with similar potencies (IC5o= 342.88 pg/mL and 129.64 pg/mL, respectively) and with lower potency the 60 mM K+-induced contraction (IC50- 24.90 pg/mL). TERP (600 pg/mL) relaxed preparations submitted to EPIN. It did not differ from that one in absence of the adrenergic mediator. At the same concentration TERP blocked the contraction induced by ACh (60 pM) in nutrient Solutions with nifedipine (10 pM) or in zero Ca2+ solution. CIN (1-1000 pg/mL) blocked the contraction induced by 60 mM K+ and with lower potency that one induced by 30 pM ACh. Also relaxed with similar potencies pre- contracted preparations that were maintained in presence ofPGF2a(30 pM) and 60 mM K+ (IC5o= 479.13 pg/mL and 78.98 pg/mL, respectively). CIN (600-1000 pg/mL) did not relax the contraction induced by 5-HT (10 pM) and at 30-600 pg/mL amplified the ACh-induced contractions. At 600 pg/mL relaxed preparations submitted to EPIN. CIN- induced relaxation was amplified by cafeine (1 mM). At 1000 pg/mL CIN amplified the contractions induced by 1.0; 3.0, and 10 mM Ca2" in 80 mM K+ and 5 mM cafeine solution and did not blocked the effects of high Ca2+ concentrations. The results of this study suggest that EOAz and TERP have antispasmodic activity on mouse respiratory smooth muscle. On the other hand it was demonstrated that CIN has a spasmogenic effect when the colinergic mediator is involved.