1 Anti-inflammatory effect and protection of rat neural stem cells
The ratio of pro-apoptotic and anti-apoptotic proteins in the Bcl-2 protein family determines whether cells undergo apoptosis after being stimulated by apoptotic signals. When the Bcl-2/Bax value decreases, Bax forms a homodimer to induce apoptosis; while when the Bcl-2/Bax value increases, Bax and Bcl-2 form a heterodimer to achieve Bcl-2 inhibition of cells function of apoptosis. Zhu Ning et al¹ found in a rat experiment that when neural stem cells were stimulated by Aβ1-42-mediated inflammatory response, the expression levels of Bcl-2 and Bax were the highest in each group, while the Bcl-2/Bax value was the highest in each group. lowest. After Hup A pretreated microglia, liquid chip detection showed that the secretion of inflammatory factors was reduced, and the Bcl-2/Bax value was significantly higher than that of Aβ group, which inhibited the apoptosis of neural stem cells. Both Western blotting and flow cytometry results indicated that Huperzine a Gnc could inhibit the apoptosis of neural stem cells.
2 Against organophosphorus neurotoxicity
The main mechanism of Huperzine a Gnc against organophosphorus poisoning is: Huperzine a Gnc is reversibly combined with acetylcholinesterase when administered in advance, thereby preventing the irreversible combination of organophosphorus compounds and acetylcholinesterase. Compared with other reversible cholinesterase inhibitors such as pyridostigmine bromide that have been used, Huperzine a Gnc has two major advantages: On the one hand, Huperzine a Gnc can pass through the blood-brain barrier, thereby protecting acetylcholinesterase in the brain. On the other hand, butyrylcholinesterase and carboxylesterase may be endogenous organophosphate scavengers. Huperzine a Gnc can selectively inhibit plasma erythrocyte acetylcholinesterase, but has no inhibitory effect on butyrylcholinesterase. Therefore, the selectivity of Huperzine a Gnc contributes to the prevention of organophosphorus poisoning.
3 Fight against glutamate toxicity
Glutamate is an agonist of N-methyl-D-aspartate (NMDA) receptors, which can increase the influx of calcium ions into neurons when NMDA receptors are stimulated, and high concentrations of calcium ions can lead to cell death . Huperzine a Gnc can reduce the toxicity of glutamate to neuronal cells and improve cell survival, especially for mature neuronal cells, which have the strongest protective effect because the number of NMDA receptors in mature neuronal cells is high. The anti-glutamate mechanism may be that after the NMDA receptor is activated, Huperzine a Gnc blocks its signal transduction channel somewhere downstream, thereby preventing the cell death caused by glutamate. In addition, the protective effect of Huperzine a Gncon nerve cells may also be There is glutamate receptor-mediated involvement.
4 Fight against oxidative stress
Huperzine a Gnc protects neuronal cells against the toxicity of beta-amyloid production and increases superoxide dismutase (SOD) production. Rat primary cortical cells cultured in vitro were incubated under the conditions of Aβ25-35 (amino acid residues 25-35 of β-amyloid fragments), and apoptosis of the cells could be observed, the cell viability was significantly decreased, and the neuronal cell morphology was changed. Alterations and their DNA fragments. Pre-administration of Huperzine a Gnc can significantly improve cell viability and prevent nuclear fragmentation. The mechanism is that Huperzine a Gnc inhibits the formation of reactive oxygen species (ROS reactive oxygen species) and the activity of caspase-3.
5 Inhibits the neurotoxicity of NO
Studies have shown that NO can inhibit the growth of human neurocytoma SK-N-SH cells and induce cell apoptosis. Huperzine a Gnc, ginkgolide A and B could block the apoptosis and growth inhibition of SK-N-SH cells by sodium nitroprusside (NO donor). In addition, Huperzine a Gnc and ginkgolides A and B also inhibited NO production in mouse glial cells and NO production in human and murine astrocytes.
