Additionally, the disfiguring scars caused by Leishmania keep patients hidden. An

estimated 1.5 million new cases of cutaneous leishmaniasis and 500,000 cases of visceral leishmaniasis occur annually, with approximately 12 million people currently infected [1]. Moreover, cases of Leishmania and human immunodeficiency virus co-infection are becoming more frequent [2, 3]. Leishmania (Leishmania) amazonensis infection results in diverse clinical manifestations, ranging from cutaneous to mucocutaneous or visceral involvement [4]. This is attributable to the genetic diversity of L. amazonensis strains, and this divergence extends to variations PFT�� solubility dmso of chromosome size [5]. The arsenal of drugs available for treating Leishmania infections is limited. The basic treatment consists of administering pentavalent antimonial compounds [6]. However, the choice

of medication depends Talazoparib on the species involved and type of clinical manifestation [7]. The usefulness of antileishmanial drugs has been limited by their toxicity, and treatment failure is often attributable to drug resistance [8]. To solve this problem, developing less toxic drugs and discovering cellular and molecular markers in parasites to identify the phenotype of chemoresistance against leishmanicidal drugs are necessary [8, 9]. These problems led to the development of additional antileishmanial drugs. Some drug-delivery systems, plants, and synthetic compounds are being developed as effective treatments for the disease [7]. Previous studies demonstrated the in vitro activity of parthenolide, a sesquiterpene lactone purified from Tanacetum parthenium, against promastigotes and intracellular Selleck GDC-0449 amastigotes (inside J774G8 macrophages) of L. amazonensis[10].

Moreover, significant Y-27632 2HCl alterations in promastigote forms were demonstrated by light microscopy and scanning and transmission electron microscopy [11]. We evaluated the activity of parthenolide against L. amazonensis axenic amastigotes and demonstrated a possible mechanism of action of this compound in this life stage of the parasite. Results Antileishmanial assays The addition of 4.0 μM parthenolide to the culture of axenic amastigotes induced growth arrest and partial cell lysis after 48 h (i.e., growth inhibition up to 90%). When the cells were treated with 2.0 μM parthenolide, the percentage of growth inhibition was approximately 70%. Parthenolide had an IC50 of 1.3 μM and IC90 of 3.3 μM after 72 h incubation (Figure 1A). Figure 1 Effects of parthenolide (A) and amphotericin B (B) on the growth of L. amazonensis axenic amastigotes. After treatment with different concentrations of the drugs, parasites were counted, and the percentage of parasite growth inhibition was determined daily for 120 h. The data indicate the average of the two independent experiments performed twice. Statistical analysis: the data of each incubation period were compared statistically at p < 0.05.