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34367-04-9

中文名稱 人參皂苷RO
英文名稱 GinsenosideRo
CAS 34367-04-9
分子式 C48H76O19
分子量 957.11
MOL 文件 34367-04-9.mol
更新日期 2024/12/20 18:42:04
34367-04-9 結(jié)構(gòu)式 34367-04-9 結(jié)構(gòu)式

基本信息

中文別名
竹節(jié)參苷V
竹節(jié)參皂苷V
人參皂苷RO
人參皂苷RO對照品,
人參皂苷RO(標(biāo)準(zhǔn)品)
人參皂苷RO(分析標(biāo)準(zhǔn)品)
人參皂苷RO、 竹節(jié)參苷V
人參皂苷RO/竹節(jié)參苷V 標(biāo)準(zhǔn)品
人參皂苷ROGINSENOSIDE RO
英文別名
PolysciasaponinP3
HericiuMsaponin S3
Chikusetusaponin V
ChikusetsusaponinV
Chikusetsusaponin 5
Ginseng Extract – Ginsenoside
28-(β-D-Glucopyranosyloxy)-28-oxoolean-12-en-3β-yl 2-O-β-D-glucopyranosyl-β-D-glucopyranosiduronic acid
3β-(2-O-β-D-Glucopyranosyl-β-D-glucopyranuronosyloxy)oleana-12-ene-28-oic acid 28-β-D-glucopyranosyl ester
28-(β-D-Glucopyranosyloxy)-28-oxo-5α-olean-12-en-3β-yl 2-O-β-D-glucopyranosyl-β-D-glucopyranosiduronic acid
β-D-Glucopyranosiduronic acid, (3β)-28-(β-D-glucopyranosyloxy)-28-oxoolean-12-en-3-yl2-O-β-D-glucopyranosyl-
所屬類別
生物化工:提取物

物理化學(xué)性質(zhì)

外觀性狀白色粉末,易溶于甲醇乙醇,來源于人參。
沸點(diǎn)1018.6±65.0 °C(Predicted)
密度1.14
儲存條件Store at 2-8°C, protect from light
溶解度DMSO : 100 mg/mL (104.48 mM; Need ultrasonic)
酸度系數(shù)(pKa)2.76±0.70(Predicted)
形態(tài)粉末
顏色白色

安全數(shù)據(jù)

危險性符號(GHS)GHS hazard pictograms
GHS07
警示詞警告
危險性描述H302
海關(guān)編碼29389090

應(yīng)用領(lǐng)域

用途1
用于含量測定/鑒定/藥理實(shí)驗(yàn)等。
藥理藥效:人參主要具有大補(bǔ)元?dú)?,滋補(bǔ)強(qiáng)壯,安神益智,生津,復(fù)脈固脫等功效。
用途2
人參皂苷Ro是人參根莖的主要皂苷成分,有抗炎癥、抗肝炎等生物活性。
人參皂苷RO價格(試劑級)
報價日期產(chǎn)品編號產(chǎn)品名稱CAS號包裝價格
2024/11/08S9103人參皂苷RO
Ginsenoside Ro
34367-04-91mg1204.38元

常見問題列表

生物活性
Ginsenoside Ro (Polysciasaponin P3; Chikusetsusaponin 5; Chikusetsusaponin V) 具有 Ca2+ 拮抗劑的抗血小板作用,IC50 為 155? μM。Ginsenoside Ro 降低 TXA2 產(chǎn)量,Ginsenoside Ro 還稍弱地降低 COX-1 和 TXAS 活性。
靶點(diǎn)

TXA 2

Ca 2+

體外研究

Ginsenoside Ro in Panax ginseng is a beneficial novel Ca 2+ -antagonistic compound and may prevent platelet aggregation-mediated thrombotic disease. Ginsenoside Ro dose-dependently reduces thrombin-stimulated platelet aggregation, and IC 50 is approximately 155?μM. Ginsenoside Ro inhibits TXA 2 production to abolish thrombin-induced platelet aggregation. Thromboxane A 2 (TXA 2 ) induces platelet aggregation and promotes thrombus formation. Ginsenoside Ro dose-dependently (50-300 μM) reduces the TXB 2 level that is induced by thrombin; Ginsenoside Ro (300 μM) inhibits the thrombin-mediated elevation in TXB 2 level by 94.9%. COX-1 activity in the absence of Ginsenoside Ro (negative control) is 2.3±0.1 nmol/mg protein. However, Ginsenoside Ro dose-dependently (50-300 μM) reduces its activity; at 300 μM, COX-1 activity is reduced by 26.4% of that of the negative control. TXA 2 synthase (TXAS) activity in the absence of Ginsenoside Ro (negative control) is 220.8±1.8 ng/mg protein/min. However, Ginsenoside Ro dose-dependently (50-300 μM) reduces its activity; at 300 μM, TXAS activity is reduced by 22.9% of that of the negative control. The inhibitory effect of Ginsenoside Ro (300 μM) on TXB 2 production (94.9%) is significantly higher than those on COX-1 (26.4%) and TXAS (22.9%) activities. To assess the toxicity of Ginsenoside Ro in Raw 264.7 cells, they are first treated with various concentrations (10 μM, 50 μM, 100 μM, and 200 μM) of Ginsenoside Ro for 24 h. Ginsenoside Ro exhibits no significant dose dependent toxicity. The effect of Ginsenoside Ro is next determined on cell viability and ROS levels, a marker of oxidative stress, following treatment with 1 μg/mL LPS. LPS reduces cell viability by ~70% compared with nontreated controls. Pretreatment with 100 μM and 200 μM Ginsenoside Ro for 1 h prior to 1 μg/mL LPS incubation for 24 h leads to a significant increase in cell viability. The changes in ROS levels and NO production are consistent with the effects of Ginsenoside Ro on viability.

體內(nèi)研究

Ginsenoside Ro dissolved in water is administrated by gavage to mice at doses of 25 and 250?mg/kg/day for 4 days before i.v. injection of HT29 in order to keep blood concentrations of Ginsenoside Ro above a certain level before HT29 i.v. injection followed by 40 days of oral administration of Ginsenoside Ro to the mice. After 38 days of treatment, the animals are euthanized, and the number of pulmonary metastatic nodules is counted in addition to evaluation of toxicity of Ginsenoside Ro and mouse pathology by HT29. Ginsenoside Ro (250?mg/kg/day) produces a significant decrease in the number of tumor nodules on the lung surface, yielding inhibition rates of 88% (P [4] .

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