Cimicifugoside H1
Cimicifugoside H1 shows the protective function to cerebral neuron during cerebral ischemia.
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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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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Zhongguo Zhong Yao Za Zhi. 2009 Aug;34(15):1930-4.
Cycloartane triterpenoid of Cimicifuga foetida.[Pubmed:
19894537]
To study cycloartane triterpenoid of Cimicifuga foetida and their osteoclast inhibition activity.
METHODS AND RESULTS:
The compounds were isolated and purified by normal and reversed phase column chromatographic methods. Structures were identified by spectroscopic analyses. Their osteoclast inhibition activity was then studied.Thirteen cycloartane triterpenoids were isolated from the rhizomes of C. foetida and were characterized as 25-O-acetyl-cimigenol (1), cimigenol (2), cimicidanol (3), 26-deoxyactein (4), asiaticoside A (5), 23-epi-26-deoxyactein (6), actein (7), 12beta-hydroxycimigenol (8), cimiside E (9), (23R, 24S) 25-O-acetyl-cimigenol-3-O-beta-D-xylopyranoside (10), (23R, 24S) cimigenol-3-O-beta-D-xylopyranoside (11), Cimicifugoside H1 (12) and Cimicifugoside H2 (13).
CONCLUSIONS:
Compound 5 was isolated from this genus for the first time, compound 7 was isolated firstly from the plant and compound 2, 7, 10 and 11 exhibit osteoclast inhibition activity.
Chin. J. Pathophysiol.,2016,32(5): 831-835.
Effect of cimicifugoside H-1 on amino acid neurotransmitters in striatum of rats with cerebral ischemia.[Reference:
WebLink]
To study the neuroprotective effect of Cimicifugoside H1 and to explore the mechanism involved by determining the variation of amino acid neurotransmitters in extracellular fluid in the striatum of rats with cerebral ischemia.
METHODS AND RESULTS:
The rats were randomly divided into sham-operated, cerebral ischemia, high-, middle- and low-dose Cimicifugoside H1, and ginkgo groups. Focal cerebral ischemia model was established by middle cerebral artery occlusion (MCAO) with sutures. Normal saline was intraperitoneally injected into the rats in sham-operated group and cerebral ischemia group, while ginkgo and different doses of Cimicifugoside H1 were injected into the rats in ginkgo group and high-, middle- and low-dose Cimicifugoside H1 groups, respectively, once a day for 7 d. The striatal fluids were gained in vivo by brain microdialysis. The contents of aspartic acid, glutamic acid, glycine and γ-aminobutyric acid were tested by high-performance liquid chromatography electrochemical detector system. Compared with sham-operated group, the contents of excitatory amino acids (aspartic acid and glutamic acid) were significantly increased 2 h after cerebral ischemia (P<0.05). Compared with cerebral ischemia group, the contents of aspartic acid and glutamic acid were significantly decreased 2 h after cerebral ischemia in high-dose Cimicifugoside H1 and ginkgo groups (P<0.05). Compared with cerebral ischemia group, the contents of aspartic acid and glutamic acid did not show significant decrease 2 h after cerebral ischemia in middle- and low-dose Cimicifugoside H1 groups. Compared with sham-operated group, the contents of inhibitory amino acid (γ-aminobutyric acid and glycine) were significantly decreased 3 h after cerebral ischemia in cerebral ischemia group (P<0.05). Compared with cerebral ischemia group, the contents of γ-aminobutyric acid and glycine were significantly increased 3 h after cerebral ischemia in high-dose Cimicifugoside H1 and ginkgo groups (P<0.05). Compared with cerebral ischemia group, the contents of γ-aminobutyric acid and glycine did not show significant decrease 3 h after cerebral ischemia in middle- and low-dose Cimicifugoside H1 groups.
CONCLUSIONS:
Cimicifugoside H1 restrains the excessive releases of excitatory amino acids and increases the contents of inhibitory amino acids during cerebral ischemia. It doesn't only penetrate through the blood brain barrier, but also regulates the disorder of excitatory amino acid during cerebral ischemia, thus showing the protective function to cerebral neuron during cerebral ischemia.
