Huperzine A CAS 102518-79-6
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- Appearance: Yellow-brown powder
- Purity: 99. 0%min
- Stock: In stock
- Sample: Available
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Huperzine A: The Complete Guide
Huperzine A for Sale
Basic Info of Huperzine A
Huperzine Potassium A; Huperzine A; Huperzine A extract; Perzine A; (5R,9R,11E)-5-amino-11-ethylidene-5,6,9,10- Tetrahydro-7-methyl-5,9-methylenecyclooctano(B)pyridin-2(1H)one
What is Huperzine A?
Huperzine A is a natural plant extract. Compared with similar AD treatment drugs approved by the US FDA, Huperzine A has a unique chemical structure and has extremely high selectivity to inhibit acetylcholinesterase in the brain and enhance cholinergic in the brain. function of neurons. In addition, Huperzine A has obvious effects on improving memory and improving cognitive ability.
Huperzine A has a small relative molecular weight, high lipid solubility, and is easy to pass through the blood-brain barrier. After entering the central nervous system, it is mostly distributed in the frontal lobe, temporal lobe, hippocampus and other parts of the brain. Its pharmacological effects have multiple targets. In addition to inhibiting the activity of acetylcholinesterase, it can also antagonize oxidative stress and apoptosis induced by β-amyloid peptide (Aβ), hydrogen peroxide and other neurotoxins, by activating the protein kinase C (PKC) signal transduction pathway. Activation of α-secretase promotes the decomposition of β-amyloid precursor protein (APP) in a non-amyloidogenic manner to produce sAPPα, reducing Aβ-mediated toxicity, while sAPPα can effectively promote cell proliferation, axonal growth, and protect nerves. cell.
Huperzine A Uses
Huperzine A has a highly selective inhibitory effect on acetylcholinesterase, thereby reducing the hydrolysis of acetylcholine, and by activating N receptors or M receptors on presynaptic membranes and antagonizing M receptors on postsynaptic membranes, choline Enhanced functionality. In addition, by supplementing acetylcholine precursors, the synthesis of acetylcholine is increased, and the cholinergic neurons are excited, thereby enhancing the learning and memory ability of AD patients and improving the cognitive and behavioral function. There are various molecular subtypes of acetylcholinesterase. There are G4 and G1 types in the mammalian brain. G4 type is the main type, and about 60% to 90% are distributed in the extracellular fluid of nerves, especially in the synaptic space.
Zhao et al. compared the inhibitory effects of huperzine A, tacrine, donepezil, rivastigmine and physostigmine on different subtypes of AChE in rat intracranial cortex, hippocampus and striatum. The inhibitory effect of A on G4-type acetylcholinesterase is significantly stronger than that of G1-type, that is, Huperzine A has a higher affinity for G4-type. It can be seen that Huperzine A can fully inhibit acetylcholinesterase in the synaptic cleft of acetylcholinergic neurons, increase the concentration of acetylcholine, and has a more obvious improvement effect on cognitive impairment and memory loss in AD patients.
Neuroprotective Effects of Huperzine A
Huperzine A (Hup A), in addition to its significant cholinesterase inhibitory effect, also has extensive neuroprotective effects. Its protective effect also plays an important role in the treatment of AD and against the damage of neurotoxic substances.
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 homodimers to induce cell apoptosis; when the Bcl-2/Bax value increases, Bax and Bcl-2 form heterodimers, causing Bcl-2 to inhibit cells. Apoptotic function. Zhu Ning et al.¹ found in rat experiments that when neural stem cells were stimulated by Aβ1-42-mediated inflammatory response, the expression of Bcl-2 and Bax was the highest in each group, and the Bcl-2/Bax value was the highest in each group. lowest. After pretreating microglia with Hup A, liquid phase chip detection found that the secretion of inflammatory factors was reduced. At the same time, the Bcl-2/Bax value was significantly higher than that in the Aβ group, which inhibited the apoptosis of neural stem cells. Both Western blotting and flow cytometry results indicate that Hup A can inhibit the apoptosis of neural stem cells.
The main mechanism of Hup A against organophosphorus poisoning is: Hup A reversibly binds to 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, Hup A has two major advantages: On the one hand, Hup A can pass the blood-brain barrier, thereby protecting acetylcholinesterase in the brain. On the other hand, butyrylcholinesterase and carboxylesterase may be endogenous organophosphorus scavengers. Hup A can selectively inhibit plasma erythrocyte acetylcholinesterase but has no inhibitory effect on butyrylcholinesterase. Therefore, the selectivity of Hup A contributes to the prevention of organophosphorus poisoning.
Glutamate is an agonist of N-methyl-D-aspartate (NMDA) receptors. Excitation of NMDA receptors can increase the influx of calcium ions into neurons, and excessive calcium ion concentration can lead to cell death. . Hup A can reduce the toxicity of glutamate to nerve cells and improve cell survival rate. It has the strongest protective effect on mature neuron cells, because mature neuron cells have a larger number of NMDA receptors. The mechanism of antagonizing glutamate may be that after NMDA receptor stimulation, Hup A blocks its signal transduction channel somewhere downstream, thereby preventing cell death caused by glutamate. In addition, Hup A’s protective effect on nerve cells may also be There is glutamate receptor-mediated involvement.
Hup A protects neuronal cells against the toxicity produced by beta-amyloid 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 protein fragments). Cell apoptosis can be observed, cell viability is significantly reduced, and neuronal cell morphology changes. changes and fragments of its DNA. Early administration of Hup A can significantly improve cell survival rate and prevent nuclear fragmentation. The mechanism is that Hup A inhibits the formation of reactive oxygen species (ROS reactive oxygen species) and the activity of caspase-3 enzyme.
Studies have shown that NO can inhibit the growth of human neurocytoma SK-N-SH line cells and induce cell apoptosis. Hup A, ginkgolactone A and B can block the apoptosis and growth inhibitory effects of sodium nitroprusside (NO donor) on SK-N-SH cells. In addition, Hup A and ginkgolactone A and B can also inhibit the production of NO in mouse glial cells and the production of NO in human and mouse astrocytes.
- Huperzine A – WikiPedia
- Zhang Lei et al. Research progress of huperzine A. Chinese Herbal Medicine. 2005, 36(9):1422-1426.
- Lim WH, Goodger JQ, Field AR, Holtum JA, Woodrow IE (September 2010). “Huperzine alkaloids from Australasian and southeast Asian Huperzia”. Pharmaceutical Biology.
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Huperzine A for Sale
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