Some effects of a chrysin bromide-derivative on GABA-A receptors and on Caenorhabditis elegans.

Infections by helminths are one of the major health problems in developing countries. Fast adaptation of parasitic organisms has conferred resistance to drug therapies used for decades (Burns et al., 2015), causing a threat to control worm parasites and generating an urgent need for new emergent molecules with therapeutic potential, in particular for nematodes. The nematode Caenorhabditis elegans is phylogenetically-related to parasitic species of helminths in which high throughput assays are challenging; thus, this species is an excellent model to study and evaluate novel anthelmintic drugs (Gilleard, 2004; Yoon et al., 2006). One interesting molecular target for drug development are the GABA receptors of parasitic helminths which are evolutionarily preserved in invertebrates and vertebrates and are present in C. elegans (Castillo et al., 1967; del Castillo et al., 1964; Jorgensen, 2005). GABA receptors from C. elegans are ionotropic channels that belong to the Cys-loop superfamily of ligand gated ion channels widely spread in multiple species, including humans (Olsen and Sieghart, 2008).