Neurological Effects of Honey: Current and Future Prospects
The putative neuroprotective mechanism of honey and its polyphenols. The generation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) increases irrespective of neurodamaging insults that lead to oxidative stress. The dysfunction of the antioxidant defense system synergistically causes reactive species accumulation, leading to oxidative stress. The ultimate outcome of such oxidative stress is neuronal cell death through an inflammatory, apoptotic, or necrotic response [111–114, 116, 119]. Honey (H) and its polyphenol constituents (HP) can counter oxidative stress by limiting the generation of reactive species as well as by strengthening the cellular antioxidant defense system. Honey and several honey polyphenols (apigenin, ferulic acid, and catechin) prevent neuronal cell death by attenuating neuroinflammation and apoptosis. However, the neuroinflammatory responses overlap with apoptosis, and the role of honey in necrotic cell death remains unclear. X = stop or prevent and + = improve or intensify.