Neurotrophic, anti-neuroinflammatory, and redox balance mechanisms of chalcones

摘要

The passage of time that evoke aging; the tilted redox balance that contribute oxidative entropy; the polarization of microglia cells that produce inflammatory phenotype; all represent the intricacies of CNS-dependent disease progression. Neurological diseases that result from CNS injury raise social concerns and the available therapeutic strategies are frustrated by low efficacy, high toxicity, and multiple side effects. However, emergent studies have shown the neumprotective role of natural compounds - including chalcones - with high efficacy in the protection of CNS structures. These compounds reportedly demonstrate neurotrophic mechanism through the upregulation of neurotrophic factors, anti-apoptotic Bcl-2, and downregulation of Box protein; anti-neuroinflammatory mechanism via the inhibition of neuroinflammatory pathways, attenuated secretion of pro-inflammatory cytokines, prevention of blood brain barrier (BBB) disruption, and protection against nerve senescence; antioxidant mechanism through the upregulation of Nrf2 activities, inhibition of Keapl, synthesis of antioxidant enzymes, and maintenance of high antioxidant/oxidant ratio. All these mechanisms represent chalcones' neuropmtective mechanisms. In this review, we highlight different pathways involved in CNS-related diseases and elucidate various mechanisms by which chalcones can perturb these shunts as a potential therapeutic modality.