Abstract
Panax notoginseng (Burk) F. H. Chen, as traditional Chinese medicine, has a long history of high clinical value, such as anti-inflammatory, anti-oxidation, inhibition of platelet aggregation, regulation of blood glucose and blood pressure, inhibition of neuronal apoptosis, and neuronal protection, and its main ingredients are Panax notoginseng saponins (PNS). Currently, Panax notoginseng (Burk) F. H. Chen may improve mental function, have anti-insomnia and anti-depression effects, alleviate anxiety, and decrease neural network excitation. However, the underlying effects and the mechanisms of Panax notoginseng (Burk) F. H. Chen and its containing chemical constituents (PNS) on these depression-related or anxiety-related diseases has not been completely established. This review summarized the antidepressant or anxiolytic effects and mechanisms of PNS and analyzed network targets of antidepressant or anxiolytic actions with network pharmacology tools to provide directions and references for further pharmacological studies and new ideas for clinical treatment of nervous system diseases and drug studies and development. The review showed PNS and its components may exert these effects through regulating neurotransmitter mechanism (5-HT, DA, NE), modulation of the gamma-amino butyric acid (GABA) neurotransmission, glutamatergic system, hypo-thalamus-pituitary-adrenal (HPA) axis, brain-derived neurotrophic factor (BDNF), and its intracellular signaling pathways in the central nervous system; and produce neuronal protection by anti-inflammatory, anti-oxidation, or inhibition of neuronal apoptosis, or platelet aggregation and its intracellular signaling pathways. Network target analysis indicated PNS and its components also may have anti-inflammatory and anti-apoptotic effects, which leads to the preservation of brain nerves, and regulate the activity and secretion of nerve cells, exerting anti-depression and anxiolytic effects, which may provide new directions for further in-depth researches of related mechanisms.
Highlights
Depression is a chronic and recurrent syndrome of mood disorder with significant and lasting low mood [1,2,3,4]
Ginsenoside Rg1 significantly reversed increase of serum corticosterone induced by chronic mild stress (CMS), increased the phosphorylation of cAMP response element-binding protein (CREB) in rat cerebral amygdala induced by chronic unpredictable mild stress (CUMS), up-regulated expression of brain-derived neurotrophic factor (BDNF) in the hippocampus [32,43,45], and down-regulated serum corticosterone lever [43]
Based on reported researches of each component above, including ginsenoside Rg1, Rg3, Rg5, Rb1, Rb3, Re, Rh1, Rh2, Ro, pseudoginsenoside-F(11), ginsenoside K, and notoginsenoside R1, the structures and target properties of 12 active ingredients among them was obtained from the PubChem database, shown as Table 3; network targets of antidepressant, anxiolytic actions, or other pharmacological effects were analyzed with network pharmacology tools
Summary
Depression is a chronic and recurrent syndrome of mood disorder with significant and lasting low mood [1,2,3,4]. PNS or single compounds exerted antidepressant-like effects by regulating the release of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, or anti-inflammatory cytokines IL-4 and IL-10 [10,20,29,31,32,36,48,49,50,51,52,53,54,55,56]. Such breakthroughs have been made to determine there are antidepressant effects on estrogen in the human body. This review summarized the antidepressant or anxiolytic effects and mechanisms of PNS and analyzed network targets of antidepressant or anxiolytic actions with network pharmacology tools, to provide reference for further pharmacological studies and new ideas for clinical treatment of nervous system diseases and drug studies and development
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