No abstract

No abstract

Petiveria alliacea L. (tipi), a shrub from Phytolaccaceae family is a perennial, subligneous, upstanding herbaceous, with characteristic garlicky odour and slender, compressed, semi-erect, mounting branches. Leaves present short petioles and are alternate, membranous, entire, sharp or acuminating at the apex and narrowing at the base. Flowers are sessile, reduced and on lean bracteate ears. The fruit is capsular, reduced and cuneiform. 1,2) Indigenous to the Amazon Rainforest and widely distributed in other areas including tropical America, the Caribbean, Africa, Sri Lanka, and the south-eastern Unites States.3,4) It was brought by slaves to Brazil where it is popularly known as tipi, pipi, guine root, erva-pipi, anamu, apacin, garlic guinea henweed. 3,5) This plant is commonly used for several medicinal purposes. The roots in decoction or powder and the infusion of leaves, is employed as antispasmodic, antirheumatic (topic use), anti-inflammatory, 6) antinociceptive, 7) hypoglycemiant and abortifacient. 8,9) They are reputed as sudorific, anti-venereal, diuretic, sedative, antihelminthic, emmenagogue, stimulant, anesthetic and depurative. [8][9][10] Tipi was used in religious ceremony by slaves, who called the herb "to tame the master" a reference to its toxic and sedative properties. The chief pharmacologic activities of tipi (already identified in a preliminary report) relates to the areas of infectology, rheumatology and oncology.This plant contains a diversity of biologically active compounds such as essential oil (Petiverina), saponinic glicosides, isoarborinol-triterpene, isoarborinol-acetate, isoarborinolcinnamate, steroids, alkaloids, flavonoids and tannins. [11][12][13] Acoording to the literature, the tipi root chemical analysis have revealed coumarins, benzyl-hydroxy-ethyl-trisulfide, benzaldehyde, benzoic acid, dibenzyl trisulphide, potassium nitrate, b-sitosterol, isoarborinol, isoarborinol acetate, isoarborinol cinnamate, polyphenols, trithiolaniacine, glucose and glycine. 8)The recently reported studies of Benevides et al.,14) who isolated di-n-propyl disulfide, benzyl hydroxymethyl sulfide and several other antifungal polysulfides from the roots of Petiveria alliacea L., as well as the work of Szczepanski et al. 12)Dibenzyl trisulphide, a main lipophilic compound in Petiveria alliacea L., has interesting biological activities, affecting, in addition to immunomodulation, microtubule-dependent cellular events and tyrosine phosphorylation-mediated MAP kinase signalling. 15,16) Petiveria alliacea L. is included in the Brazilian and Paraguay Pharmacopoeias and by the Japanese Directory of Drugs.The purpose of the present study was to evaluate the antinociceptive effect of the acetate (FA), hexanic (FH), hydroalcoholic (FHA) and precipitated hydroalcoholic (FHAppt) fractions of Petiveria alliacea L. in different experimental models of nociception in mice. MATERIALS AND METHODS Plant MaterialThe roots of tipi were collected in Pentecoste, state of Ceará, and brought to the Department of Organic Chemist...

A mixture of triterpenes named a-and b-amyrin (AMI), isolated from the Brazilian medicinal herb Protium hetaphyllum (Aubl) March (Burseraceae), was evaluated for the ability to inhibit aggregation of human platelets induced by adenosine 5 0 -diphosphate (ADP, 1.5 and 3 mM), collagen, and arachidonic acid (AA) in vitro. The results showed that AMI significantly inhibited platelet aggregation (40, 64, and 60%) in the assay carried out with ADP (3 mM) as agonist, at the doses of 100, 150, and 200 mM, respectively. In the presence of a lower ADP concentration (1.5 mM), a 3-time higher percentage of inhibition (32%) was observed with AMI 50 mM, as compared to that seen with 3.0 mM ADP. In the test using collagen (10 mg=mL) as agonist, AMI (50, 100, and 150 mM) inhibited aggregation by 26, 47, and 39%, respectively, while in the presence of the arachidonic acid (150 mM) at the doses of 50, 100, 150, and 200 mM, it inhibited platelet aggregation by 20, 21, 25, and 27%, respectively. The lowest IC 50 value for the AMI inhibitory effect was observed with collagen (90.0 mM), followed by ADP (117.9 mM) and arachidonic acid (181.4 mM). With ADP as agonist, the anti-aggregant effect of the acetylsalicylic acid (ASA) was potentiated by AMI but not by dipyridamole. No potentiation was observed after the combination of ASA and AMI with collagen or arachidonic acid as agonists. Our results indicated that AMI possesses a platelet anti-aggregant activity in a concentration-dependent manner and probably acts on a biochemical pathway common to all the agonists tested.

No abstract

Abstract:We evaluated the neuropharmacological profile of acetylated alpha-and beta-amyrin (AcAMY) obtained by the acetylation of the isomeric mixture of alpha-and beta-amyrin isolated from Protium heptaphyllum. Male Swiss mice were administered with AcAMY (2.5, 5, 10 and 25 mg/kg, i.p.), and anticonvulsant (pentylenetrazole-and pilocarpine-induced convulsions), sedative (barbiturate-induced sleep and open field tests) and anxiolytic (elevated plus maze test) activities were studied. Results showed that AcAMY administered intraperitoneally or orally, protected the animals against pentylenetetrazole-but not against pilocarpine-induced convulsions. The drug increased both the latency to the 1 st convulsion and the latency to death. The barbiturate-induced sleeping time was also increased, as well as the ethyl ether-induced sleeping time, confirming the sedative nature of AcAMY. The acute administration of AcAMY also produced an anxiolytic effect. After the sub-chronic administration, both sedative and anxiolytic effects were manifested, at the two higher doses. Amino acids measurements in brain areas of mice treated with AcAMY (25 mg/kg, i.p., for 7 days) showed an 89% increase in tyrosine levels, in the hippocampus. In the striatum, tyrosine and taurine were increased by 97 and 79%, respectively, while decreases in the levels of aspartate, GABA and glutamate of 72, 55 and 60%, respectively were observed. In conclusion, our results showed that AcAMY presents sedative, anxiolytic and anticonvulsant properties. Although the drug mechanism of action is not completely clarified, it seems to involve a decrease in excitatory amino acids and an increase of inhibitory amino acids. Furthermore, the GABAergic system may also play a role.