Published October 31, 2022
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Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
- 1. * & Zoology, Biological and Geological Sciences Department, Faculty of Education, Alexandria University, Alexandria, Egypt
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Elkader, Heba-Tallah Abd Elrahim Abd, Essawy, Amina E., Al-Shami, Ahmed S. (2022): Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases. Phytochemistry (113293) 202: 1-16, DOI: 10.1016/j.phytochem.2022.113293, URL: http://dx.doi.org/10.1016/j.phytochem.2022.113293
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- urn:lsid:plazi.org:pub:FFAE0975FFDAFFBA9A68FFEFFFABFFCC
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- Changes in neurotransmission caused by varying the levels of neurotransmitters and related receptors have been discovered to play key roles in neurodegeneration and neuroprotection. The neuroprotective actions of saponins may be achieved by regulating neurotransmitters (Table 2). Saponins, for example, safeguard the nervous system by regulating biogenic amine neurotransmitters and modulating N-methyl- D-aspartate (NMDA), adenosine, or -aminobutyric acid (GABA) receptors, all of which are linked to enhanced neurogenesis (Xie et al., 2018). The levels of DA and 5-HT in the PFC, hippocampus, and striatum are restored after daily supplementation with A. spinosus saponin or AS-IV in combination with BPA. Thus, TH expression is activated, which potentially inhibits mitochondria-induced apoptosis and promotes neurite outgrowth.
- Saponins also help to restore neurotransmitter deficiencies by altering neurotransmitter levels, neurotransmitter receptors, and second messenger signalling pathways. As a result, saponins have diverse bioactivities (Zhang et al., 2019; Abd Elkader et al., 2021). Essawy et al. (2021) discovered that coadministration of saponins extracted from A. spinosus or AS-IV reversed NO and glutamate overproduction, and increased glutamine concentrations induced by BPA in the PFC, hippocampus, and striatum, followed by glutamate excitability, decreased Ca+2 influx, decreased glutamate excitability and decreased Ca+2 influx. Furthermore, animals administered AS-IV or A. spinosus exhibited lower expression levels of NMDA ionotropic receptor subunits (NR2A and NR2B) in brain areas impacted by BPA. This change might be due to ASIV-mediated blockade of NMDA receptors and a decrease in glutamate neural excitability (Li et al., 2017a). Saponins, on the other hand, enhanced the function of NMDA receptors through a direct competitive interaction with the receptor glycine binding site and exerted a potent inhibitory effect on excitotoxic damage by blocking the interaction of NMDA receptors with glutamate to prevent glutamate toxicity (Sun et al., 2015).