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Jujuboside A


Catalogue Number : BF-J3002
Specification : 98%
CAS number : 55466-04-1
Formula : C58H94O26
Molecular Weight : 1207.35
PUBCHEM ID : 51346169
Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

seeds of Zizyphus jujuba

Structure Type



Standards;Natural Pytochemical;API




Ziziphus jujuba Mill. Var/α-L-arabinopyranoside, (3β,16β,23R)-16,23:16,30-diepoxy-20-hydroxydammar-24-en-3-yl O-6-deoxy-α-L-mannopyranosyl-(1->2)-O-[O-β-D-glucopyranosyl-(1->6)-O-[β-D-xylopyranosyl-(1->2)]-β-D-glucopyranosyl-(1->3)]-/(3β,16β,23R)-20-Hydroxy-16,23:16,30-diepoxydammar-24-en-3-yl 6-deoxy-α-L-mannopyranosyl-(1->2)-[β-D-glucopyranosyl-(1->6)-[β-D-xylopyranosyl-(1->2)]-β-D-glucopyranosyl-(1->3)]-α -L-arabinopyranoside/jujuboside C/α-L-Arabinopyranoside, (3β,16β,23R)-16,23:16,30-diepoxy-20-hydroxydammar-24-en-3-yl O-6-deoxy-α-L-mannopyranosyl-(1->2)-O-[O-β-D-glucopyranosyl-(1->6)-O-[β-D-xylopyranosyl-(1->2)]- β-D-glucopyranosyl-(1->3)]-/JujubosideA/(3β,16β,23R)-20-Hydroxy-16,23:16,30-diepoxydammar-24-en-3-yl 6-deoxy-α-L-mannopyranosyl-(1->2)-[β-D-glucopyranosyl-(1->6)-[β-D-xylopyranosyl-(1->2)]-β-D-glucopyranosyl-(1->3)]-α-L-arabinopyranoside




1.5±0.1 g/cm3


Flash Point

Boiling Point

Melting Point



InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:55466-04-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Rationale: It has been reported that peroxisome proliferator activated receptor γ (PPARγ) level decreases significantly in the brains of Alzheimer’s disease (AD) patients and mice models, while the mechanism is unclear. This study aims to unravel the mechanism that amyloid β (Aβ) decreases PPARγ and attempted to discover lead compound that preserves PPARγ. Methods: In APP/PS1 transgenic mice and Aβ treated microglia, the interaction between HSP90 and PPARγ were analyzed by western blot. Using a PPRE (PPARγ responsive element) containing reporter cell line, compounds that activate PPARγ activity were identified. After genetic ablation or pharmacological inhibition of potential target pathways, the target of jujuboside A (JuA) was discovered through Axl/HSP90β. After oral administration or intrathecal injection, the anti-AD activity of JuA was evaluated by Morris water maze (MWM) test and object recognition test. Soluble Aβ42 levels and plaque numbers after JuA treatment were detected by thioflavin S staining, and the activation of microglia was assayed by immunofluorescence staining against Iba-1. Results: We found that Aβ stress decreased heat shock protein 90 β (HSP90β), subsequently reduced the abundance of PPARγ, and down-regulated Aβ clearance-related genes in BV2 cells and primary microglia. We identified that JuA stimulated the expression of HSP90β, strengthened the interaction between HSP90β and PPARγ, preserved PPARγ levels, and thus effectively promoted the clearance of Aβ42. We demonstrated that JuA increased HSP90β expression through Axl/ERK pathway. JuA significantly ameliorated cognitive deficiency in APP/PS1 transgenic mice, meanwhile, JuA significantly reduced the soluble Aβ42 levels and plaque numbers in the brain. Notably, the therapeutic effects of JuA were dampened by R428, an Axl inhibitor. Conclusions: This study suggests that the up-regulation of HSP90β by JuA through Axl is a potential therapeutic strategy to facilitate Aβ42 clearance and ameliorate cognitive deficiency in AD.


Alzheimer's disease; Axl; HSP90β; Jujuboside A; PPARγ; amyloid β


Jujuboside A promotes Aβ clearance and ameliorates cognitive deficiency in Alzheimer's disease through activating Axl/HSP90/PPARγ pathway.


Zhang M1, Qian C1, Zheng ZG1, Qian F1, Wang Y1, Thu PM1, Zhang X1, Zhou Y1, Tu L1, Liu Q1, Li HJ1, Yang H1, Li P1, Xu X1,2.

Publish date

2018 Jul 30




Jujuboside A (JuA), an active saponin, is responsible for the anxiolytic and sedative effects of Zizyphi Spinosae Semen (ZSS). In this study, the gastrointestinal absorption and metabolic dynamics of JuA were investigated in vivo and in vitro. The results showed that the bioavailability was 1.32% in rats, indicating only a trace amount of JuA was able to be absorbed. Further investigation revealed that its poor bioavailability was not caused by malabsorption but by the metabolic process. JuA was hydrolyzed largely in the stomach before being absorbed into the different parts of the intestine (especially duodenum and colon), and the gastric environment played a vital role in this process. Furthermore, the metabolites, jujuboside B (JuB) and jujubogenin, exhibited significant effects on the expression and activation of γ-amino-butyric acid A (GABA(A)) receptors. Our findings demonstrate that the metabolites of the saponin, not the original molecule, should be responsible for the specific bioactivities.


Jujuboside A; Zizyphi Spinosae Semen; bioavailability; intestinal absorption; metabolic dynamics


Gastrointestinal Absorption and Metabolic Dynamics of Jujuboside A, A Saponin Derived from the Seed of Ziziphus jujuba.


Song P1, Zhang Y1, Ma G1, Zhang Y1,2, Zhou A1,3, Xie J1,2.

Publish date

2017 Sep 27




Cardiomyocyte apoptosis is closely associated with the pathogenesis of heart failure. Jujuboside A (JUA) is a type of saponin isolated from the seeds of Zizyphus jujuba. In traditional Chinese medicine, it is believed that JUA possesses multiple biological effects, including antianxiety, antioxidant and anti‑inflammatory activities. The present study aimed to evaluate the effects of JUA on norepinephrine (NE)‑induced apoptosis of H9c2 cells and to investigate its underlying mechanisms. Rat H9c2 cardiomyocytes were pretreated with JUA and were then exposed to NE as an in vitro model of myocardial apoptosis. A cell viability assay, scanning electron microscopy, transmission electron microscopy, flow cytometry assay, acridine orange/ethidium bromide staining, reverse transcription‑quantitative polymerase chain reaction and western blotting, all revealed that NE induced H9c2 cell apoptosis. The results demonstrated that NE inhibited cell viability, and enhanced cell damage and apoptosis of H9c2 cells. Conversely, pretreatment with JUA was able to reverse NE‑induced decreased cell viability and increased apoptosis. Furthermore, JUA suppressed upregulation of the B‑cell lymphoma 2 (Bcl‑2)‑associated X protein/Bcl‑2 ratio, and inhibited the increased protein expression levels of cleaved caspase‑3 and cleaved caspase‑9 following NE exposure. However, the protein expression levels of cleaved caspase‑12 and cleaved caspase‑8 were not significantly altered following exposure to NE or JUA pretreatment. In addition, in JUA‑pretreated cells, the protein expression levels of phosphorylated (p)‑p38 and p‑c‑Jun N‑terminal kinase were downregulated compared with in NE‑treated cells. Furthermore, JUA regulated the activation of extracellular signal‑regulated kinase (ERK) in NE‑treated cells and significantly increased the expression levels of p‑AKT. Taken together, these data suggested that JUA may protect against NE‑induced apoptosis of cardiomyocytes via modulation of the mitogen‑activated protein kinase and AKT signaling pathways. Therefore, JUA may be considered a potential therapeutic strategy for the treatment of heart disease.


Jujuboside A attenuates norepinephrine-induced apoptosis of H9c2 cardiomyocytes by modulating MAPK and AKT signaling pathways.


Wan CR1, Han DD1, Xu JQ1, Yin P1, Xu XL2, Mei C3, Liu FH3, Xia ZF1.

Publish date

2018 Jan