Figure 1.

The hypothesis map illustrates the interplay between natural antioxidant compounds, the body’s innate antioxidant defenses, reactive oxygen species (ROS), microglial inflammatory responses, and the management of neuropsychiatric disorders. Antioxidants such as N-acetylcysteine, sulforaphane, alpha-lipoic acid, L-carnitine, ascorbic acid, selenocompounds, flavones, and zinc, etc., not only function by scavenging ROS, enhancing the activity of antioxidant enzymes, such as superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and thioredoxin (Trx), and promoting the expression of antioxidant genes such as nuclear factor erythroid 2-related factor 2 (Nrf2), but they also exert effects on specific molecular targets. For instance, N-acetylcysteine (NAC) and zinc can directly interact with N-methyl-D-aspartate (NMDA) receptors, ascorbic acid can directly affect the activity of Tet Methylcytosine Dioxygenase 2 (TET2) enzymes, and Flavonoid compounds have the ability to directly interact with tyrosine kinase receptor B (TrkB) receptors and subsequently activate downstream signaling pathways such as Phospholipase C (PLC), Extracellular Signal-Regulated Kinase (ERK), and Protein kinase B (AKT).