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Albiflorin

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-A1004

  • Specification : 98%

  • CAS number : 39011-90-0

  • Formula : C23H28O11

  • Molecular Weight : 480.46

  • PUBCHEM ID : 24868421

  • Volume : 20mg

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Catalogue Number

BF-A1004

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

480.46

Appearance

White crystalline powder

Botanical Source

Paeonia lactiflora,Paeonia anomala subsp. veitchii

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC12CC(C3CC1(C3(C(=O)O2)COC(=O)C4=CC=CC=C4)OC5C(C(C(C(O5)CO)O)O)O)O

Synonyms

7-Oxatricyclo[4.3.0.0]nonan-8-one, 9-[(benzoyloxy)methyl]-1-(β-D-glucopyranosyloxy)-4-hydroxy-6-methyl-, (1R,3R,4R,6S,9S)-/[(1R,3R,4R,6S,9S)-1-(β-D-Glucopyranosyloxy)-4-hydroxy-6-methyl-8-oxo-7-oxatricyclo[4.3.0.0]non-9-yl]methyl benzoate/Paeonia lactiflora Pall./Alibiflorin/albiflorin

IUPAC Name

[(1R,3R,4R,6S,9S)-4-hydroxy-6-methyl-8-oxo-1-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-7-oxatricyclo[4.3.0.03,9]nonan-9-yl]methyl benzoate

Applications

Albiflorin is a major constituent contained in peony root; possesses therapeutic potential for neurodegenerative diseases.IC50 value:Target: in vitro: Albiflorin significantly ameliorated Glu-induced reduction of cell viability, nuclear and mitochondrial apoptotic alteration, reactive oxygen species accumulation, and B-cell lymphoma 2 (Bcl-2)/Bax ratio. Albiflorin also enhanced phosphorylation of AKT and its downstream element glycogen synthase kinase-3β, and this effect was abrogated by the AKT inhibitor LY294002 [1]. in vivo: Mice were exposed to X-ray radiation (400 Roentgen), and both mice and rabbits were intraperitoneally injected with cyclophosphamide (100.0 mg/kg) and cytarabine chloride (92.7 mg/kg), respectively, for 3 days to induce myelosuppression. Albiflorin was subsequently administrated intravenously at low (15.0 mg/kg for mice, 6.00 mg/kg for rabbits), intermediate (30.0 mg/kg for mice, 12.0 mg/kg for rabbits) and high (60.0 mg/kg for mice, 24.0 mg/kg for rabbits) doses, as well as orally (60.0 mg/kg for mice, 24.0 mg/kg for rabbits) for 7 days. Shenqi tablets were used as positive controls (oral administration of 936.0 mg/kg for mice, 336.0 mg/kg for rabbits). The administration of Albiflorin significantly ameliorated myelosuppression in all cases [2].

Density

1.6±0.1 g/cm3

Solubility

Methanol; Water

Flash Point

248.9±26.4 °C

Boiling Point

722.1±60.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C23H28O11/c1-21-8-13(25)12-7-23(21,33-19-17(28)16(27)15(26)14(9-24)32-19)22(12,20(30)34-21)10-31-18(29)11-5-3-2-4-6-11/h2-6,12-17,19,24-28H,7-10H2,1H3/t12-,13+,14+,15+,16-,17+,19-,21-,22-,23-/m0/s1

InChl Key

QQUHMASGPODSIW-RPLHGOISSA-N

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:39011-90-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28732574

Abstract

Objective: Brown adipose tissue (BAT) activation has been identified as a possible target to treat obesity and to protect against metabolic diseases by increasing energy consumption. We explored whether albiflorin (AF), a natural compound, could contribute to lowering the high risk of obesity with BAT and primary brown preadipocytes in vivo and in vitro.
Materials/methods: Human adipose tissue-derived mesenchymal stem cells (hAMSCs) were cultured with adipogenic differentiation media with or without AF. Male C57BL/6J mice (n=5 per group) were fed a high-fat diet (HFD) for six weeks with or without AF. Brown preadipocytes from the interscapular BAT of mice were cultured with or without AF.
Results: In white adipogenic differentiation of hAMSCs, AF treatment significantly reduced the formation of lipid droplets and the expression of adipogenesis-related genes. In HFD-induced obese C57BL/6J mice, AF treatment significantly reduced body weight gain as well as the weights of the white adipose tissue, liver and spleen. Furthermore, AF induced the expression of genes involved in thermogenic function in BAT. In primary brown adipocytes, AF effectively stimulated the expressions of thermogenic genes and markedly up-regulated the AMP-activated protein kinase (AMPK) signaling pathway. Pretreatment with phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 nullified the induction of the thermogenic genes by AF in primary brown adipocytes. Moreover, AF activated beige cell marker genes induced by the pharmacological activation of peroxisome proliferator-activated receptor γ in hAMSCs.
Conclusion: This study shows that AF prevents the development of obesity in hAMSCs and mice fed an HFD and that it is also capable of stimulating the differentiation of brown adipocytes through the modulation of thermogenic genes by AMPK and PI3K/AKT.

KEYWORDS

Albiflorin; Brown adipose tissue; High-fat diet-induced obesity; Thermogenic gene; hAMSCs.

Title

Albiflorin Ameliorates Obesity by Inducing Thermogenic Genes via AMPK and PI3K/AKT in Vivo and in Vitro

Author

Mi-Young Jeong 1 , Jinbong Park 2 , Dong-Hyun Youn 2 , Yunu Jung 2 , JongWook Kang 2 , Seona Lim 2 , Min-Woo Kang 2 , Hye-Lin Kim 2 , Hong-Seob So 3 , Raekil Park 4 , Seung-Heon Hong 5 , Jae-Young Um 6

Publish date

2017 Aug

PMID

30371044

Abstract

Background: Foam cells are characteristic pathologic cells of atherosclerosis (AS), they are lipid-loaded macrophages present on atherosclerotic lesions. A large number of studies has shown that the pathogenesis of AS is the result of interactions between the lipid metabolism disorders and chronic inflammatory responses in the body. Albiflorin can inhibit the inflammatory response and it has shown a therapeutic effect on certain inflammatory diseases.
Methods: In this study, a human acute monocytic leukemia cell line (THP-1)-derived foam cell model was established via oxidized low-density lipoprotein (ox-LDL) to observe the effects of albiflorin on the AS-characteristic foam cells.
Results: Our results showed that, after the treatment with ox-LDL, macrophages induced by propylene glycol methyl ether acetate (PMA), presented large amounts of lipid deposition in their cytoplasm, indicating that the THP-1-derived foam cell model was successfully established. On the other hand, the same cells pretreated with albiflorin presented significantly reduced amounts of lipid deposition, and their contents of total cholesterol and triglyceride were also clearly lower. Besides, the expression levels of low-density lipoprotein receptor-1 (LOX-1) and nuclear factor-κB (NF-κB) were significantly decreased, and the expression levels of downstream factors interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were also obviously decreased in the cells treated with albiflorin but not in the negative control cells. Moreover, after treatment of macrophages with different concentrations of ox-LDL, the expression levels of LOX-1 and NF-κB were up-regulated in an ox-LDL concentration-dependent manner, and so were the expression levels of IL-6 and TNF-α. And, it was found after treatment with LOX-1 neutralizing antibody or NF-κB inhibitor (during the foam cell formation induction via ox-LDL) that the lipid deposition in the cytoplasm of the cells was reduced, as in the cells treated with albiflorin.
Conclusions: Taken together, our findings suggest that albiflorin decreases lipid deposition in the cytoplasm and blocks the foaming process by regulating the LOX-1/NF-κB signaling pathway.

KEYWORDS

Albiflorin; Brown adipose tissue; High-fat diet-induced obesity; Thermogenic gene; hAMSCs.

Title

Albiflorin Inhibits the Formation of THP-1-derived Foam Cells Through the LOX-1/NF-κB Pathway

Author

Jiyou Sun 1 , Xiaojuan Li 2 , Kai Jiao 3 , Zhiwei Zhai 4 , Dajun Sun 5

Publish date

2019 Apr

PMID

31150651

Abstract

Albiflorin, the main component of Radix Paeoniae Alba, has been shown to ameliorate injury in cell models of Alzheimer’s disease induced by amyloid-β (Aβ), but the mechanism is unclear. We used 7-month-old APP/PS1 mice to determine whether albiflorin is capable of protecting against Alzheimer’s disease. We found that four weeks of intragastric administration of albiflorin (20 mg/kg/d and 40 mg/kg/d) ameliorated memory deficits in APP/PS1 mice. Albiflorin conferred synaptic protection by decreasing Aβ levels and increasing PSD-95, synaptophysin and synapsin 1 levels in the brains of APP/PS1 mice. Albiflorin played an antioxidative role by reducing reactive oxygen species (ROS) levels and elevating Mn-SOD activity in the brain. Albiflorin also reduced the level of Drp1, increased the levels of Mfn1, Mfn2 and Opa1 and improved mitochondrial morphology in APP/PS1 mice. Albiflorin inhibited the mitochondrial pathway of apoptosis by increasing the levels of Bcl-2 and Bcl-xl and decreasing the levels of Bax, caspase-3 and cytochrome c in both the hippocampus and the cortex and by reducing the number of apoptotic cells in the anterior parietal cortex of the APP/PS1 mice. In conclusion, treatment with albiflorin improved mitochondrial function, reduced Aβ deposition in the brain and ameliorated memory deficits in APP/PS1 mice. These findings indicate that albiflorin may serve as a potential antidementia drug.

KEYWORDS

APP/PS1 mice; Albiflorin; Amyloid-β; Mitochondrial dysfunction; Reactive oxygen species.

Title

Albiflorin Ameliorates Memory Deficits in APP/PS1 Transgenic Mice via Ameliorating Mitochondrial Dysfunction

Author

Yi-Jun Xu 1 , Yu Mei 1 , Xue-Qing Shi 1 , Yi-Fang Zhang 1 , Xin-Yue Wang 2 , Li Guan 1 , Qi Wang 3 , Hua-Feng Pan 4

Publish date

2019 Sep 15