Tuberculosis is an extremely serious problem of global public health. Its incidence is worsened by the presence of multidrug-resistant (MDR) strains of Mycobacterium tuberculosis. More serious forms of drug resistance have been observed in recent years. Therefore, the discovery and/or synthesis of new potent and less toxic anti-tubercular compounds is very critical, especially having in mind the consequences and the delays in treatment caused by the COVID-19 pandemic. Enoyl-acyl carrier protein reductase (InhA) is an important enzyme involved in the biosynthesis of mycolic acid, a major component of the M. tuberculosis cell wall. At the same time, it is a key enzyme in the development of drug resistance, making it an important target for the discovery of new antimycobacterial agents. Many different chemical scaffolds, including hydrazide hydrazones and thiadiazoles, have been evaluated for their InhA inhibitory activity. The aim of this review is to evaluate recently described hydrazide-hydrazone- and thiadiazole-containing derivatives that inhibit InhA activity, resulting in antimycobacterial effects. In addition, a brief review of the mechanisms of action of currently available anti-tuberculosis drugs is provided, including recently approved agents and molecules in clinical trials.

The hepatoprotective potential of saponarin, isolated fromGypsophila trichotoma, was evaluatedin vitro/in vivousing a hepatotoxicity model of paracetamol-induced liver injury. In freshly isolated rat hepatocytes, paracetamol (100 μmol) led to a significant decrease in cell viability, increased LDH leakage, decreased levels of cellular GSH, and elevated MDA quantity. Saponarin (60–0.006 μg/mL) preincubation, however, significantly ameliorated paracetamol-induced hepatotoxicity in a concentration-dependent manner. The beneficial effect of saponarin was also observedin vivo. Rats were challenged with paracetamol alone (600 mg/kg, i.p.) and after 7-day pretreatment with saponarin (80 mg/kg, oral gavage). Paracetamol toxicity was evidenced by increase in MDA quantity and decrease in cell GSH levels and antioxidant defence system. No changes in phase I enzyme activities of AH and EMND and cytochrome P 450 quantity were detected. Saponarin pretreatment resulted in significant increase in cell antioxidant defence system and GSH levels and decrease in lipid peroxidation. The biochemical changes are in good correlation with the histopathological data. Protective activity of saponarin was similar to the activity of positive control silymarin. On the basis of these results, it can be concluded that saponarin exerts antioxidant and hepatoprotective activity against paracetamol liver injuryin vitro/in vivo.

Amorpha fruticosa L. (Fabaceae) is a shrub native to North America which has been cultivated mainly for its ornamental features, honey plant value and protective properties against soil erosion. It is registered amongst the most noxious invasive species in Europe. However, a growing body of scientific literature also points to the therapeutic potential of its chemical constituents. Due to the fact that A. fruticosa is an aggressive invasive species, it can provide an abundant and cheap resource of plant chemical constituents which can be utilized for therapeutic purposes. Additionally, exploitation of the biomass for medicinal use might contribute to relieving the destructive impact of this species on natural habitats. The aim of this review is to provide a comprehensive summary and systematize the state-of-the-art in the knowledge of the phytochemical composition and the potential of A. fruticosa in disease treatment and prevention, with especial emphasis on diabetes and metabolic syndrome. Also reviewed are aspects related to potential toxicity of A. fruticosa which has not yet been systematically evaluated in human subjects.