辽东楤木皂苷VII 340982-22-1价格

产品中文名称：   辽东楤木皂苷VII 340982-22-1价格

中文别名：   辽东楤木皂甙VII 

英文名：   Araloside VII 

英文别名：   Congmunoside VII 

CAS登录号：   340982-22-1 

分子式：   C54H88O24 

分子量：   1120 

辽东楤木皂苷VII 340982-22-1价格分子结构：  

  

外观：   白色粉末 

规格：   20 mg/支 

纯度：   ≥ 98% 

用途：   用于含量测定/鉴定/药理实验等。 

提取来源：   五加科楤木属辽东楤木(Aralia elate(Miq.)Seem．) 的根 

溶解性：   可溶于水，不溶于石油醚、***、二氯甲烷等有机溶剂。 

药理药效：   补气安神、 强精滋肾、 祛风HX、ZL神经衰弱。 

贮存条件：   4℃冷藏、密封、避光 

有效期：   2年 

辽东楤木皂苷VII 340982-22-1价格标准品和对照品的本质区别：

所谓标准品，即是标准物品，作为一种衡量标准，如果用在药物方面，则为含量测定中的标准含量。标准品包括化学计量标准品、冶金标准品和药检标准品。采用生化方法来测定，目前国家规定的标准品共有15种，林可酶素、新霉素、大观酶素、太乐菌素、链霉素、卡那霉素、绒促性素、盐酶素、杆菌肽锌、安普酶素、红霉素、合成缩宫素、庆大霉素、渡毛化苷G。

所谓对照品，是指用于鉴别、检查、含量测定和校正检定仪器性能的标准物质。采用化学方法来测定，即是一般仪器的都叫做对照品，国家规定的有107种，包括地塞米松、土霉素、阿莫西林等等。

刺五加皂苷B和对照品一样是指国家药品标准中用于鉴别、检查、含量测定、杂质和有关物质检查等标准物质，它是国家药品标准不可分割的组成部分。

但刺五加皂苷B和对照品又是两个不同的概念，ZG药典凡例中有明确的定义：刺五加皂苷B是指用于生物鉴定、抗生素或生物药品中含量或效价测定的标准物质，以效价单位（U）表示，而对照品系指用于鉴别、检查、含量测定和校正检定仪器性能的标准物质。文献中经常混淆了这两个概念，认为刺五加皂苷B就是对照品，是同种物质的不同提法，之所以会有这样的误解，可能是有的药品既有刺五加皂苷B，又有对照品。例如，非那西丁当用作熔点校准物质时，用熔点刺五加皂苷B，测定含量时，用对照品；当用微生物法测定头孢克罗效价时，用头孢克罗刺五加皂苷B，用HPLC或U刺五加皂苷B法测定时，则用对照品。

辽东楤木皂苷VII 340982-22-1价格特点：是一种敏感性高,特异性强,重复性好的实验诊断方法，由于其试剂稳定、易保存,操作简便,结果判断较客观等因素,已广泛应用在免疫学检验的各领域中。

检测方式：相色谱法HPLC≥98%。

贮存条件：4℃冷藏、密封、避光。

包装：可根据客户需求提供相应批量包装。

用途：用于含量测定、鉴别、药理实验、活性筛选等。

Proteolytically cleaved by caspases during neuronal apoptosis. Cleavage at Asp-739 by either caspase-6, -8 or -9 results in the production of the neurotoxic C31 peptide and the increased production of beta-amyloid peptides.

N- and O-glycosylated. O-linkage of chondroitin sulfate to the L-APP isoforms produces the APP proteoglycan core proteins, the appicans. The chondroitin sulfate chain of appicans contains 4-O-sulfated galactose in the linkage region and chondroitin sulfate E in the repeated disaccharide region.

Phosphorylation in the C-terminal on tyrosine, threonine and serine residues is neuron-specific. Phosphorylation can affect APP processing, neuronal differentiation and interaction with other proteins. Phosphorylated on Thr-743 in neuronal cells by Cdc5 kinase and Mapk10, in dividing cells by Cdc2 kinase in a cell-cycle dependent manner with maximal levels at the G2/M phase and, in vitro, by GSK-3-beta. The Thr-743 phosphorylated form causes a conformational change which reduces binding of Fe65 family members. Phosphorylation on Tyr-757 is required for SHC binding. Phosphorylated in the extracellular domain by casein kinases on both soluble and membrane-bound APP. This phosphorylation is inhibited by heparin.

Extracellular binding and reduction of copper, results in a corresponding oxidation of Cys-144 and Cys-158, and the formation of a disulfide bond. In vitro, the APP-Cu(+) complex in the presence of hydrogen peroxide results in an increased production of beta-amyloid-containing peptides. Trophic-factor deprivation triggers the cleavage of surface APP by beta-secretase to release sAPP-beta which is further cleaved to release an N-terminal fragment of APP (N-APP).

Beta-amyloid peptides are degraded by IDE.

DISEASE : Defects in APP are the cause of Alzheimer disease type 1 (AD1) [MIM:104300]. AD1 is a familial early-onset form of Alzheimer disease. It can be associated with cerebral amyloid angiopathy. Alzheimer disease is a neurodegenerative disorder characterized by progressive dementia, loss of cognitive abilities, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major constituent of these plaques is the neurotoxic amyloid-beta-APP 40-42 peptide (s), derived proteolytically from the transmembrane precursor protein APP by sequential secretase processing. The cytotoxic C-terminal fragments 

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