Abstract
Se evaluó el ácido úsnico (1), aislado del liquen Evernia prunastri (Cajamarca-Perú), producto natural conocido por sus actividades biológicas, y, del mismo modo, se evaluó la síntesis de su derivado acil-hidrazona (2), obtenido a partir de una reacción de condensación entre el ácido úsnico y la isoniazida en solución etanólica a reflujo, con un rendimiento global de 95%. Ambos compuestos fueron evaluados y comparados con la isoniazida según su actividad anti-Mycobacterium tuberculosis basada en el ensayo de susceptibilidad mediante el método TEMA. Los resultados mostraron que el compuesto 1 presenta valores de MIC de 16,0 μg/mL frente a las cepas H37Rv, TB DM 97 y MDR DM 1098, mientras que el compuesto 2 presenta valores de MIC de 2,0; 64,0 y 64,0 μg/mL respectivamente.
Highlights
Tuberculosis (TB), caused by the bacteria Mycobacterium tuberculosis, is a major public health problem that annually kills approximately 3 million people worldwide
The therapy against tuberculosis is based on the use of combined drugs such as rifampicin, isoniazid (INH), and pyrazinamide, which are employed as components of currently applied multidrug therapy of TB [3]
Usnic acid [L.o g4 was obtained as yellow crystals from dried thallus of lichen Evernia prunastri [qWW g4] using repeatedly flash column chromatography with hexanekethyl acetate [N:x4 and hexanektoluenek ethyl acetate [oj:j:qj4
Summary
Tuberculosis (TB), caused by the bacteria Mycobacterium tuberculosis, is a major public health problem that annually kills approximately 3 million people worldwide. It is worsened if there is co-infection with HIV [1]. The therapy against tuberculosis is based on the use of combined drugs such as rifampicin, isoniazid (INH), and pyrazinamide, which are employed as components of currently applied multidrug therapy of TB [3]. MDR-TB includes the strains resistant to at least isoniazid and rifampin, considered as the more efficient first-line drugs against TB. The occurrence of mutations within several genes is responsible for the MDR-phenotype. In the case of INH resistance, mutations within katG, inhA, ahpC, kasA, genes are involved [4]
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