29838-67-3
基本信息
落妇新苷
落新妇苷对照品,
落新妇苷(标准品)
落新妇苷(落新妇甙)
落新妇苷(分析标准品)
落新妇苷, 来源于土茯苓
紫杉叶3-O鼠李甲基酸酯
ASTILBIN 落新妇苷
ASTILBIN 落新妇苷 标准品
Taxifolin 3-rhaMnoside
Taxifolin 3-o-rhamnoside
Dihydroquercetin 3-rhamnoside
Astilbin Taxifolin 3-O-rhaMnoside
Astilbin, 98%, from Smilax glabra Roxb.
Astilbin froM Engelhardtia roxburghiana
(2R,3R)-2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4-oxo-3,4-dihydro-2H-chroMen-3-yl 6-deoxy-alpha-L-Mannopyranoside
(2R,3R)-3-[(6-Deoxy-alpha-L-mannopyranosyloxy)]-2-(3,4-dihydroxy-phenyl)-2,3-dihydro-5,7-dihydroxy-4H-chromen-4-one
(2R,3R)-2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-3-[(2S,3R,4R,5S,6S)-3,4,5-trihydroxy-6-methyl-oxan-2-yl]oxy-chroman-4-one
物理化学性质
| 外观性状 | 白色结晶粉末，易溶于沸水，几乎不溶于乙醚，来源于土茯苓、菝葜，黄杞Engelhardtia roxburghiana Wall.红绒毛羊蹄甲。 |
| 熔点 | 180 °C (decomp) |
| 沸点 | 801.1±65.0 °C(Predicted) |
| 密度 | 1.74 |
| 储存条件 | 2-8°C |
| 溶解度 | 水中的溶解度为1mg/mL，透明，无色 |
| 酸度系数(pKa) | 7.34±0.60(Predicted) |
| 形态 | A crystalline solid |
| 颜色 | White to off-white |
| InChIKey | ZROGCCBNZBKLEL-MQGABXIONA-N |
| SMILES | O([C@]1([H])O[C@@H](C)[C@H](O)[C@@H](O)[C@H]1O)[C@H]1C(C2=C(C=C(O)C=C2O[C@@H]1C1C=CC(O)=C(O)C=1)O)=O |&1:1,4,6,8,10,12,22,r| |
安全数据
| 危险性符号(GHS) |  GHS09 |
| 警示词 | 警告 |
| 危险性描述 | H400 |
| 防范说明 | P273 |
| 危险品标志 | N |
| 危险类别码 | 50 |
| 安全说明 | 61 |
| 危险品运输编号 | UN 3077 9 / PGIII |
| WGK Germany | 3 |
| 海关编码 | 29389090 |
应用领域
常见问题列表
土茯苓为百合科植物光叶菝锲(Smilax glabra Roxb.)的干燥根茎，它是一种常用中药材，具有除湿，解毒通利关节的作用。 紫杉叶3-O鼠李甲基酸酯(astilbin)是土茯苓中分离得到的一种黄酮类化合物，具有杀虫，抑制辅酶A还原酶，抑制醛糖还原酶，保肝，镇痛，抗水肿，抗氧化等活性作用。
紫杉叶3-O鼠李甲基酸酯还能显著改善免疫性肝损伤，诱导PHA活化的Jurkat细胞凋亡，通过抑制活化T淋巴细胞的功能来抑制迟发型超敏反应和治疗小鼠胶原型关节炎等。
落新妇苷（Astilbin）是一种黄酮类化合物，可从 Smilax glabra 根茎中分离。Astilbin 增强 NRF2 活化。Astilbin 还抑制 TNF-α 表达和 NF-κB 活化。
|
TNF-α
|
NF-κB
|
NRF2
|
Astilbin is a common dietary flavonoid that can be found in various kinds of herbs and foods such as Smilax Glabra , Sarcandra glabra , grape and red wine. Astilbin markedly inhibits cisplatin-induced cell apoptosis and recovers cell growth. Astilbin significantly decreases reactive oxygen species (ROS) accumulation and alleviates ROS-induced activation of p53, MAPKs and AKT signaling cascades, which in turn attenuates cisplatin-induced HEK-293 cell apoptosis. Astilbin effectively enhances NRF2 activation and transcription of its targeting antioxidant genes to reduce ROS accumulation in cisplatin-induced HEK-293 cells. Astilbin obviously suppresses tumor necrosis factor alpha (TNF-α) expression and NF-κB activation, and also inhibits the expression of induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). To measure the effects of Astilbin on the growth of CDDP-treated renal cells, HEK-293 cells are treated with CDDP (100 μM) and/or Astilbin (200 μM). Astilbin treatment significantly improvescell growth in CDDP-induced HEK-293 cells.
To explore whether Astilbin improves CDDP-induced nephrotoxicity in vivo, an acute cisplatin nephrotoxic mouse model is established. Single injection of CDDP with 8 mg/kg dose results in notable weight loss compared with control group. However, the phenomenon is significantly alleviated by Astilbin at dose of 50 mg/kg. The mice fed Astilbin alone do not show any obvious alteration in body weight. Similarly, serum creatinine (SCr) and blood urea nitrogen (BUN) are higher in CDDP-treated mice than in control group. Treatment with Astilbin also decreases SCr and BUN levels. To examine the protective effect of Astilbin on CDDP-induced renal histopathological damage, the mouse kidney sections are stained with H&E. The mice in control group and Astilbin treated group have normal kidney morphology, while kidneys in CDDP group show severe damage with tubular degeneration, necrosis and cystic dilatation of the tubules with focal hemorrhages. Administration of Astilbin mitigated kidney injury, resulting in lower histopathological score compared to CDDP group. The apoptosis of renal cells is also detected using TUNEL staining to determine whether Astilbin treatment decreased renal cell apoptosis in CDDP-induced acute nephrotoxic mice.