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Forsythoside E


Catalogue Number : BD-P0027
Specification : 98.0%(HPLC)
CAS number : 93675-88-8
Formula : C20H30O12
Molecular Weight : 462.44
PUBCHEM ID : 69634125
Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Forsythia suspensa

Structure Type



Standards;Natural Pytochemical;API




β-L-Glucopyranoside, 2-(3,4-dihydroxyphenyl)ethyl 6-O-(6-deoxy-α-L-mannopyranosyl)-/2-(3,4-Dihydroxyphenyl)ethyl 6-O-(6-deoxy-α-L-mannopyranosyl)-β-L-glucopyranoside/DecaffeoylforsythosideA




1.6±0.1 g/cm3


Methanol; Water

Flash Point

408.6±32.9 °C

Boiling Point

752.0±60.0 °C at 760 mmHg

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#:93675-88-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




Individuals with Crohn’s disease frequently require ileocecal resection (ICR), and inflammation often recurs in the neoterminal ileum following surgery. Fructooligosaccharide (FOS) is a fermentable prebiotic that stimulates the growth of bifidobacteria and may promote anti-inflammatory activity. The aim of this study was to determine if supplementation of a postICR diet with FOS in a mouse model would be effective in stimulating the growth of bifidobacteria and reducing systemic and local inflammation.

ICR was performed in IL10-/- mice (129S1/SvlmJ) with colitis. Following surgery, nonICR control and ICR mice were fed a chow diet ± 10% FOS for 28 days. Serum, colon, and terminal ileum (TI) were analyzed for cytokine expression by MesoScale discovery platform. DNA extracted from stool was analyzed using 16s rRNA sequencing and qPCR. Expression of occludin and ZO1 was assessed using qPCR. Short-chain fatty acid (SCFA) concentrations were assessed using gas chromatography.

ICR led to increased systemic inflammation (P < 0.05) and a significant decline in fecal microbial diversity (P < 0.05). Mice on the FOS diet had a greater reduction in microbial diversity and also had worsened inflammation as evidenced by increased serum IL-6 (P < 0.05) and colonic IFNγ and TNFα (P < 0.05). Expression of occludin and ZO1 were significantly reduced in FOS-supplemented mice. There was a correlation between loss of diversity and the bifidogenic effectiveness of FOS (r = -0.61, P < 0.05). Conclusions FOS-supplementation of a postICR diet resulted in a decrease in fecal bacterial diversity, reduction in barrier function, and increased gut inflammation.


experimental models, fructooligosaccharide, microbiome, surgery, Crohn’s disease


Prebiotic Supplementation Following Ileocecal Resection in a Murine Model is Associated With a Loss of Microbial Diversity and Increased Inflammation


Michael Laffin, MD,1 Troy Perry, MD, PhD,1 Heekuk Park, PhD,2,3 Naomi Hotte, MSc,3 Richard N Fedorak, MD,2,3 Aducio Thiesen, MD, PhD,4 Bryan Dicken, MD,1 and Karen L Madsen, PhD2,3

Publish date

2018 Jan;




Due to the high water content of cartilage, hydrostatic pressure is likely one of the main physical stimuli sensed by chondrocytes. Whereas, in the physiological range (0 to around 10 MPa), hydrostatic pressure exerts mostly pro-chondrogenic effects in chondrocyte models, excessive pressures have been reported to induce detrimental effects on cartilage, such as increased apoptosis and inflammation, and decreased cartilage marker expression. Though some genes modulated by high pressure have been identified, the effects of high pressure on the global gene expression pattern have still not been investigated. In this study, using microarray technology and real-time PCR validation, we analyzed the transcriptome of ATDC5 chondrocyte progenitors submitted to a continuous pressure of 25 MPa for up to 24 h. Several hundreds of genes were found to be modulated by pressure, including some not previously known to be mechano-sensitive. High pressure markedly increased the expression of stress-related genes, apoptosis-related genes and decreased that of cartilage matrix genes. Furthermore, a large set of genes involved in the progression of osteoarthritis were also induced by high pressure, suggesting that hydrostatic pressure could partly mimic in vitro some of the genetic alterations occurring in osteoarthritis.


High hydrostatic pressure induces pro-osteoarthritic changes in cartilage precursor cells: A transcriptome analysis


Kevin Montagne, Conceptualization, Formal analysis, Investigation, Validation, Visualization, Writing - original draft, Writing - review & editing,1,* Yasuko Onuma, Formal analysis, Funding acquisition, Investigation, Resources, Writing - review & editing,2 Yuzuru Ito, Formal analysis, Funding acquisition, Investigation, Resources, Writing - review & editing,2 Yasuhiko Aiki, Formal analysis, Investigation, Resources,2 Katsuko S. Furukawa, Funding acquisition, Project administration, Writing - review & editing,1,3 and Takashi Ushida, Funding acquisition, Project administration, Supervision, Writing - review & editing1,3,

Publish date





The steadily increasing epidemic of obesity continues at alarming rates, is an important public health problem, and expression changes of S100A16 and 11 β-hydroxysteroid dehydrogenase type 1(11β-HSD1) is attributable to the adipocyte differentiation. In our previous study, we found that 11β-HSD1 protein expression increased in S100A16-overexpressed 3T3-L1 cell model. In order to further investigate the relationship between S100A16 and 11β-HSD1, and the molecular mechanisms of S100A16-induced adipogenesis, we constructed S100A16 transgenic and knockout mouse, and S100A16-overexpressed 3T3-L1 preadipocyte cell. Using S100A16 transgenic (S100A16Tg/+) mice fed with normal fat diet (NFD) and high fat diet (HFD) diet model, we evaluated the effect of S100A16 on adipogenesis, expression of 11β-HSD1, and RNA sequencing and quantification of gene expression. Using the 3T3-L1 cell model, we examined the effect of S100A16 and 11β-HSD1 on pre-adipocyte differentiation, and cell signaling events of 11β-HSD1 overexpression induced by S100A16. We found that when compared with C57BL/6 mice, overexpression of S100A16 under the condition of HFD increased lipid content in WAT and fat infiltration in hepatocytes, 11β-HSD1 protein expression increased along with S100A16. Elevated S100A16 and 11β-HSD1 expression promoted adipogenesis in 3T3-L1 cells. Overexpression of S100A16 inhibited the degradation of 11β-HSD1. We conclude that S100A16-induced adipogenesis is associated with up-regulation of 11β-HSD1.


11β-HSD1, adipogenesis, obesity, S100A16, type 2 diabetes


S100A16-induced adipogenesis is associated with up-regulation of 11 β-hydroxysteroid dehydrogenase type 1 (11β-HSD1)


Rihua Zhang,1 Jing Bao Kan,1 Shan Lu,1 Pei Tong,1 Jie Yang,1 Ling Xi,1 Xiubing Liang,2 Dongming Su,2 Dong Li,3 and Yun Liu1

Publish date

2019 Sep 30;