RESUMEN
PURPOSE: Leishmaniasis is an infectious disease transmitted by insects that proliferate mainly in impoverished environments of tropical climates. In the absence of an effective vaccine, pharmacological treatment is the main tool to combat this disease. The objective of this work was to analyze the anti-leishmanial activity of 2-chloro-N-[4-(4-chlorophenyl)-2-thiazolyl] acetamide (AT) in promastigotes of Leishmania mexicana. METHODS: The biological activity of the compound was evaluated using a sulphorhodamine B cytotoxicity test and the integrity of the erythrocytes was evaluated by a lysis test. The anti-trypanosomatid activity was evaluated in vitro, a cell death assay was performed by flow cytometry (IP/Annexin V stain) and a parasite growth recovery assay was performed. RESULTS: The AT showed a CC50 value of 0.031 µM for HeLa cells after 24 h of exposure, which did not induce erythrocyte lysis. On the other hand, the AT showed an IC50 value of 0.086 µM for L. mexicana (promastigote form) after 24 h of interaction. The compound was capable of inducing apoptosis in the parasites and did not allow recovery after 24 h of exposure. CONCLUSION: This study provides valuable information with the objective of developing new drugs for the treatment of this disease, although more research on this molecule is needed to improve its biological activity.
Asunto(s)
Antiprotozoarios , Leishmania mexicana , Leishmaniasis , Acetamidas/uso terapéutico , Antiprotozoarios/farmacología , Antiprotozoarios/uso terapéutico , Apoptosis , Células HeLa , HumanosRESUMEN
BACKGROUND: Adjuvants have been obtained empirically by trial and error experiments and today, there is a tendency to the rational design of adjuvants candidates, which will increasingly achieve effective and safe products. The aim of this work was to design and evaluate the compound IMR-23 derived from nitroimidazole as an immunomodulatory molecule. MATERIALS AND METHODS: The IMR-23 molecule was obtained by a condensation reaction, cytotoxicity was tested by the sulforhodamine B assay. Adjuvanticity was evaluated in vivo and in vitro in J774A.1 cells and in the mouse model, respectively. RESULTS: IMR-23 that did not show cytotoxicity on HeLa, Vero cells and macrophages J774A.1, was able to induce the production of molecules involved in the inflammatory process, such as cytokines and chemokines determined by ELISA, to induce the production of antibodies and to generate antigenspecific cells to ovalbumin and against the antigen GST-L1b. CONCLUSION: These results open the possibility of further studies to obtain a proper balance of immunogenicity- toxicity in the use of IMR-23 as an adjuvant molecule.