Hirsuteine
Hirsuteine exhibits potent neuroprotective effects against glutamate-induced HT22 cell death. Hirsuteine non-competitively antagonizes nicotine-evoked dopamine release by blocking ion permeation through nicotinic receptor channel complexes.
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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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Jpn J Pharmacol. 1993 Apr;61(4):351-6.
Non-competitive antagonism by hirsuteine of nicotinic receptor-mediated dopamine release from rat pheochromocytoma cells.[Pubmed:
8320880]
Effects of Hirsuteine, an indole alkaloid extracted from Uncaria genus, on nicotine- and high K-induced responses were investigated in rat pheochromocytoma PC12 cells.
METHODS AND RESULTS:
Hirsuteine (300 nM-10 microM) inhibited dopamine release evoked by 100 microM nicotine in a concentration-dependent manner. Hirsuteine did not produce a parallel shift of the concentration-response relationship curve for nicotine, but reduced maximal dopamine release. Dopamine release evoked by 60 and 155 mM KCl was also inhibited by Hirsuteine, but the concentration necessary for significant inhibition was higher (more than 10 microM). Under whole cell voltage-clamp, Hirsuteine reversibly inhibited inward currents activated by 100 microM nicotine. The current inhibition was slightly accelerated by hyperpolarization.
CONCLUSIONS:
The results suggest that Hirsuteine non-competitively antagonizes nicotine-evoked dopamine release by blocking ion permeation through nicotinic receptor channel complexes. The blockade of Ca channels, which are activated during nicotine-evoked depolarization, may not play a major role in the antagonism.
J Asian Nat Prod Res. 2014;16(8):876-83.
Alkaloids from the hook-bearing branch of Uncariarhynchophylla and their neuroprotective effects against glutamate-induced HT22 cell death.[Pubmed:
24899363]
METHODS AND RESULTS:
One new alkaloid, 4-geissoschizine N-oxide methyl ether (1), was isolated from the EtOH extract of the hook-bearing branch of Uncariarhynchophylla, together with 10 known alkaloids, 3-epi-geissoschizine methyl ether (2) isolated from U.rhynchophylla for the first time, geissoschizine methyl ether (3), 4-Hirsuteine N-oxide (4), Hirsuteine (5), hirsutine (6), 3α-dihydro-cadambine (7), 3β-isodihydro-cadambine (8), cadambine (9), strictosamide (10), and akuammigine (11). The structures were elucidated by spectroscopic methods including UV, ESI-QTOF MS, NMR, and circular dichroism experiments. Neuroprotective effects of 1-9 were investigated against 3 mM glutamate-induced HT22 cell death.
CONCLUSIONS:
The activity assay showed that 2, 3, 5, and 6 exhibited potent neuroprotective effects against glutamate-induced HT22 cell death. However, only weak neuroprotective activities were observed for 1, 4, 7, 8, and 9.
