Anemoside A3
Anemoside A3 is an attractive candidate for further development as a cognitive enhancer capable of alleviating memory dysfunctions associated with aging and neurodegenerative diseases. Anemoside A3 also produces relaxation in rat renal arteries through multiple mechanisms.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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Neuropsychopharmacology. 2015 Jul;40(8):1877-87.
Anemoside A3 Enhances Cognition through the Regulation of Synaptic Function and Neuroprotection.[Pubmed:
25649278]
Compounds that have the ability to both strengthen synaptic function and facilitate neuroprotection are valuable cognitive enhancers that may improve health and quality of life, as well as retard age-related cognitive deterioration. Medicinal plants are an abundant source of potential cognitive enhancers.
METHODS AND RESULTS:
Here we report that Anemoside A3 (AA3) isolated from Pulsatilla chinensis modulates synaptic connectivity in circuits central to memory enhancement. Anemoside A3 specifically modulates the function of AMPA-type glutamate receptors (AMPARs) by increasing serine phosphorylation within the GluA1 subunit, which is a modification required for the trafficking of GluA1-containing AMPARs to synapses. Furthermore, Anemoside A3 administration activates several synaptic signaling molecules and increases protein expressions of the neurotrophin brain-derived neurotrophic factor and monoamine neurotransmitters in the mouse hippocampus. In addition to acting through AMPARs, Anemoside A3 also acts as a non-competitive NMDA receptor (NMDAR) modulator with a neuroprotective capacity against ischemic brain injury and overexcitation in rats. These findings collectively suggest that AA3 possesses a unique ability to modulate the functions of both AMPARs and NMDARs. Concordantly, behavioral studies indicate that AA3 not only facilitates hippocampal long-term potentiation but also enhances spatial reference memory formation in mice.
CONCLUSIONS:
These multifaceted roles suggest that Anemoside A3 is an attractive candidate for further development as a cognitive enhancer capable of alleviating memory dysfunctions associated with aging and neurodegenerative diseases.
Planta Med. 2003 Feb;69(2):171-4.
Pulsatilloside A and anemoside A3 protect PC12 cells from apoptosis induced by sodium cyanide and glucose deprivation.[Pubmed:
12624827]
METHODS AND RESULTS:
Using sodium cyanide (NaCN) and glucose deprivation induced cell injury in PC12 as an injury model, we investigated the protective effects of pulsatilloside A and anemoside A 3 on neurons. The results showed that PC12 cells under the NaCN-injury and glucose deprivation would undergo apoptosis. Additions of pulsatilloside A and anemoside A 3, at dosages ranging from 0.1, 1 and 10 microg/ml, protected PC12 cells from apoptosis determined by MTT, LDH release analysis, and flow cytometry measurement.
Planta Med. 2010 Nov;76(16):1814-9.
Anemoside A3-induced relaxation in rat renal arteries: role of endothelium and Ca2+ channel inhibition.[Pubmed:
20506075]
Anemoside A3, a lupane-type triterpenoid saponin, exists in the roots of Pulsatilla chinensis, but its pharmacological properties are largely unknown.
METHODS AND RESULTS:
The present study aimed to investigate the mechanisms underlying Anemoside A3 induced relaxation in rat renal arteries. Changes of isometric force were determined on arteries with a myograph. Anemoside A3 caused concentration-dependent relaxation in precontracted aortas, mesenteric, left coronary, and renal arteries. Removal of endothelium or treatment with charybdotoxin plus apamin slightly but significantly attenuated the relaxation in renal arteries. TEA(+) inhibited the relaxation caused by Anemoside A3 in renal arteries with and without endothelium while glibenclamide, BaCl(2), or capsaicin had no effect on it. Anemoside A3 produced less relaxation in rings contracted by 60 mM KCl compared with rings contracted by receptor-dependent constrictors. It further inhibited contractions induced by Ca(2+) influx through nifedipine-sensitive voltage-gated Ca(2+) channels, nifedipine-insensitive receptor-operated Ca(2+) channels, and by intracellular Ca(2+) release. Pretreatment with nifedipine attenuated Anemoside A3-induced relaxation.
CONCLUSIONS:
Taken together, the present results indicate that Anemoside A3 produces relaxation in rat renal arteries through multiple mechanisms. The release of CTX/apamin-sensitive endothelium-derived hyperpolarizing factor, stimulation of TEA(+)-sensitive K(+) channel, and inhibition of Ca(2+) influx jointly contribute to the relaxation.
