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52286-74-5

中文名稱 人參皂苷 Rg2
英文名稱 Ginsenoside Rg2
CAS 52286-74-5
分子式 C42H72O13
分子量 785.03
MOL 文件 52286-74-5.mol
更新日期 2024/12/24 17:23:08
52286-74-5 結(jié)構(gòu)式 52286-74-5 結(jié)構(gòu)式

基本信息

中文別名
人參皂莢RG2
人參皂苷-RG2
(R型)人參皂苷
人參皂苷RG2(S)
(S型)人參皂苷RG2
人參皂苷RG2(標(biāo)準(zhǔn)品)
人參皂苷20(S)-RG2
S-人參皂苷RG2,人參皂甙RG2
人參皂苷RG2/20(S)-人參皂苷RG2
GINSENOSIDE RG2 人參皂苷RG2
英文別名
anaxatriol
GinsesideRg2
Panaxoside Rg2
product/154570
Ginsenosdie Rg2
PROSAPOGENIN C2
GINSENOSIDE RG2
mannopyranosyl)-
iGInsenoside Rg2
GINSENOSIDE Rg2(SH)
所屬類別
生物化工:提取物

物理化學(xué)性質(zhì)

外觀性狀白色結(jié)晶粉末,可溶于甲醇、乙醇、DMSO等有機(jī)溶劑,來源于人參、西洋參。
熔點(diǎn)187~189℃
沸點(diǎn)881.0±65.0 °C(Predicted)
密度1.30±0.1 g/cm3(Predicted)
儲存條件2-8°C
溶解度甲醇(微溶、加熱、超聲處理)、吡啶(微溶、超聲處理)
酸度系數(shù)(pKa)12.85±0.70(Predicted)
形態(tài)固體
顏色白色至灰白色
穩(wěn)定性吸濕性
InChIKeyAGBCLJAHARWNLA-DJZXLMSJSA-N
LogP6.830 (est)

安全數(shù)據(jù)

危險(xiǎn)性符號(GHS)GHS hazard pictograms
GHS07
警示詞警告
危險(xiǎn)性描述H302
防范說明P301+P312+P330
危險(xiǎn)品標(biāo)志Xn
危險(xiǎn)類別碼22
安全說明24/25
WGK Germany3
RTECS號LZ6430000
海關(guān)編碼29389090
毒性mouse,LD50,intraperitoneal,1340mg/kg (1340mg/kg),Arzneimittel-Forschung. Drug Research. Vol. 25, Pg. 343, 1975.

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:夠增強(qiáng)心肌的收縮力,增加心輸出量,同時增強(qiáng)缺血心肌血流量。
用途2
(20S)-人參皂苷Rg2是富含于人參中的甾醇皂苷,具有很高的生物活性。

常見問題列表

簡介

人參皂苷 Rg2 是人參的主要活性成分之一。人參皂苷 Rg2 是一種 NF-κB 抑制劑。 人參皂苷 Rg2還降低 Aβ1-42 積聚。

人參皂苷 Rg2

作用功效

人參皂苷Rg2對急性心源性休克有保護(hù)作用,具有抗休克、抗心衰、抗凝血、抗血栓作用。主要表現(xiàn)在強(qiáng)壯心肌,增強(qiáng)心肌收縮力,減慢心率,擴(kuò)張血管,增加心輸出量和提高冠脈流量,能快速改善心肌缺血和缺氧,具有明顯的增強(qiáng)心功能作用。

生物活性
Ginsenoside Rg2 是人參的主要活性成分之一。Ginsenoside Rg2 是一種 NF-κB 抑制劑。 Ginsenoside Rg2 還降低 Aβ1-42 積聚。
靶點(diǎn)

NF-κB

1-42

體外研究

Ginsenoside Rg2 prevents the decrease of IκB expression stimulated with lipopolysaccharide (LPS). IκB dissociation from RelA-p50 complex is crucial for NF-κB activity. Ginsenoside Rg2, protopanaxatriol, inhibits vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression stimulated with LPS from human umbilical vein endothelial cell (HUVEC). The inhibition of VCAM-1 and ICAM-1 expression by Ginsenoside Rg2 is in a concentration-dependent manner, significantly. Treatment of endothelial cells with LPS (1μg/mL) decreases IκBα expression. By 1 hr after LPS treatment, significant decrease of IκBα is attained. To determine whether LPS-stimulated IκBα expression is affected by Ginsenoside Rg2, endothelial cells are treated for 1 hr with Ginsenoside Rg2 (1~50 μM) prior to LPS (1 μg/mL) stimulation for 1 hr. Ginsenoside Rg2 reverses the decrease of LPS-induced IκBα expression in a concentration-dependent manner, significantly. The adhesion of THP-1 cells to endothelial cells is measured using quantitative monolayer adhesion assay. The adhesion of THP-1 cells onto endothelial cells are increased to five folds by LPS (1 μg/mL) stimulation for 8 hrs. Ginsenoside Rg2 (1~50 μM) inhibits the adhesion of THP-1 cells to endothelial cells stimulated with LPS, in a concentration-dependent manner.

體內(nèi)研究

G-Rg1 and Ginsenoside Rg2 (G-Rg2) reduce the escape latencies on the last two training days compared to the Alzheimer's disease (AD) model group (p<0.05). In the spatial exploration test, the total time spent in the target quadrant and the number of mice that exactly crossed the previous position of the platform are clearly shorter and lower, respectively, in the AD model group mice than in the normal control group mice (p<0.01), a trend that is reversed by treatment with G-Rg1 and Ginsenoside Rg2 (G-Rg1, p<0.01; Ginsenoside Rg2, p<0.05). Treatment with G-Rg1 and Ginsenoside Rg2 effectively improve cognitive function of the mice that have declined due to AD. G-Rg1 and Ginsenoside Rg2 reduce Aβ 1-42 accumulation in APP/PS1 mice. In the G-Rg1 and Ginsenoside Rg2 treated mice, the pathological abnormalities observed in the APP/PS1 mice are gradually ameliorated. Clear nucleoli and light brown, sparsely scattered Aβ deposits are visible.

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