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  • Brand : BIOFRON

  • Catalogue Number : BF-C1018

  • Specification : 98%

  • CAS number : 85643-19-2

  • Formula : C22H26O11

  • Molecular Weight : 466.44

  • PUBCHEM ID : 158845

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystal

Botanical Source

Curculigo orchioides

Structure Type



Standards;Natural Pytochemical;API




β-D-Glucopyranoside, 2-(((2,6-dimethoxybenzoyl)oxy)methyl)-4-hydroxyphenyl/Curculigoside A/2-(β-D-Glucopyranosyloxy)-5-hydroxybenzyl 2,6-dimethoxybenzoate/Benzoic acid, 2,6-dimethoxy-, [2-(β-D-glucopyranosyloxy)-5-hydroxyphenyl]methyl ester


[5-hydroxy-2-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyphenyl]methyl 2,6-dimethoxybenzoate


1.5±0.1 g/cm3


Methanol; Ethanol; Acetone; Ethyl Acetate

Flash Point

253.8±26.4 °C

Boiling Point

734.9±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#:85643-19-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Objective: To investigate the regulation of curculigoside on osteogenic differentiation of MG63 and the protective effect on osteoporosis model mice. Methods: The effects of curculigoside on the survival rate of dexamethasone or H(2)O(2) treated MG63 were detected by methyl thiazolyl tetrazolium (MTT). The specimens were divided into six groups: blank control group, blank administration group, model group (dexamethasone or H(2)O(2) treatment group), low dose group (dexamethasone or H(2)O(2)+1.0 μmol/L curculigoside), medium dose group (dexamethasone or H(2)O(2)+2.5 μmol/L curculigoside) and high dose group (dexamethasone or H(2)O(2)+5.0 μmol/L curculigoside), the sample size of each group was 10. Western blotting was used to detect the expression of osteogenic differentiation-related proteins [type Ⅰ collagen, integrin β1, osteoblast-specific transcription factor (Osterix), osteocalcin and osteopontin] in MG63 cells after 1, 7 and 14 days incubated with 0, 1.0, 2.5 and 5.0 μmol/L of curculigoside. The sample size for each group at each time point was six. The experimental mice were divided into 4 groups: blank group, model group (dexamethasone treatment group), curculigoside low-dose group (dexamethasone+5 mg/kg curculigoside) and high-dose group (dexamethasone+45 mg/kg curculigoside), twenty each. After treatment, the tibia of the mice in each group were subjected to sacral HE staining. The number of osteoclasts was counted, and the levels of oxidative related factors in serum were determined by enzyme-linked immunosorbent assay (ELISA). Results: The MTT results showed that compared with the blank control group [(100±3.7)%], the cell survival rate decreased to (44.1±5.7)% after treatment with dexamethasone, and the survival rate increased to (79.7±3.8)% after treatment with 5.0 μmol/L of curculigoside. The cell survival rate decreased to (59.1±4.7)% after H(2)O(2) treatment, and the survival rate increased to (80.8±3.5)% after treatment with 2.5 μmol/L of curculigoside. The results of Western blotting showed that the expression of type Ⅰ collagen and integrin β1 in MG63 cells was significantly increased after 1.0, 2.5 and 5.0 μmol/L of curculigoside for 1, 7 and 14 days compared with 0 μmol/L of curculigo side for the same period. After increasing (P<0.05), the expression of Osterix and osteocalcin was significantly increased after 1 day of incubation (P<0.05). However, compared with 0 μmol/L curculigoside treatment, the expression of osteopontin in MG63 cells was not significantly different after incubation with 1.0, 2.5, 5.0 μmol/L of curculigoside for 7 and 14 days (P>0.05). Compared with the blank group, the number of tibia osteoclasts in the osteoporosis model group increased. In the low-dose and high-dose groups of curculigoside, the tibia cortex was more continuous and the number of osteoclasts decreased. Compared with the blank group, the activity of oxygen in the osteoporosis model group was significantly increased (P<0.05), and superoxide dimutase and catalase were significantly decreased (P<0.05). Conclusions: Curculigoside promotes the differentiation of MG63 cells by increasing the expression of osteoblast differentiation-related proteins, and has a certain therapeutic effect on dexamethasone-induced osteoporosis mice.


Cell differentiation; Curculigoside; Osteoblasts; Osteoporosis


[Study on the effect of curculigoside on osteoporosis].


Han RY1, Li YT, Li YY, Qiu TY, Song JY, Hu M.

Publish date

2019 Sep 9




The present study aimed to investigate the anti‑arthritic effects of curculigoside isolated from the rhizome of Curculigo orchioides Gaertn in vivo and in vitro, as well as to determine the potential underlying mechanisms. A rat model of arthritis was induced with type II collagen. Arthritic rats were treated with curculigoside (50 mg/kg) and blood samples were collected to determine serum levels of tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6, IL‑10, IL‑12 and IL‑17A. Furthermore, indices of the thymus and spleen were determined. The anti‑proliferative effects of curculigoside were detected with Cell Counting kit‑8 assays in rheumatoid arthritis‑derived fibroblast‑like synoviocyte MH7A cells. In addition, expression levels of Janus kinase (JAK)1, JAK3, signal transducer and activator of transcription (STAT)3, nuclear factor (NF)‑κB p65 and its inhibitor (IκB) were determined by western blotting. The results revealed that curculigoside inhibited paw swelling and arthritis scores in type II collagen‑induced arthritic (CIA) rats. Additionally, curculigoside decreased serum levels of TNF‑α, IL‑1β, IL‑6, IL‑10, IL‑12 and IL‑17A in CIA rats. Curculigoside also significantly inhibited MH7A cell proliferation in a time and concentration‑dependent manner. Furthermore, treatment downregulated the expression of JAK1, JAK3 and STAT3, and upregulated cytosolic nuclear factor (NF)‑κB p65 and IκB. In conclusion, the results of the present study indicated that curculigoside exhibited significant anti‑arthritic effects in vivo and in vitro, and the molecular mechanism may be associated with the JAK/STAT/NF‑κB signaling pathway.


Curculigoside exerts significant anti‑arthritic effects in vivo and in vitro via regulation of the JAK/STAT/NF‑κB signaling pathway.


Tan S1, Xu J2, Lai A2, Cui R2, Bai R2, Li S2, Liang W2, Zhang G2, Jiang S2, Liu S2, Zheng M2, Wang W2.

Publish date

2019 Mar




The present investigation found that curculigoside (CUR) can prevent excess-iron-induced bone loss in mice and cells through antioxidation and inhibiting excess-iron-induced phosphorylation of the Akt-FoxO1 pathway. CUR can attenuate the decreasing of cell viability, enhance autophagy, potentiate the antioxidant effect, and reduce apoptosis in MC3T3-E1 cells treated with excess iron through regulating the expression of FoxO1 target gene.

Oxidative stress induced by iron overload is an important factor involved in primary osteoporosis disease and iron overload-related diseases. Curculigoside (CUR), a phenolic glycoside found abundantly in Curculigo orchioides Gaertn., has been demonstrated to possess antioxidant and antiosteoporotic properties. The aim of the present study is to explore the underlying molecular mechanism of CUR on excess-iron-induced bone loss in mice and osteoblastic MC3T3-E1 cells.

An iron-overload mice model was used to study the protective effects of CUR on bone loss induced by oxidative stress. Serum bone metabolism markers and antioxidant enzymes were also measured. To explore the antioxidant mechanism of CUR, the MC3T3-E1 osteoblastic cell line was used.

In vivo studies showed that BMD and microarchitectural parameters were improved after a 3-month administration of CUR. CUR improved the biochemical parameters related to bone metabolism and the expressions of Runx2, OCN, and type 1 collagen and increased the formation of bone-mineralized nodules in vitro. CUR also inhibited ROS generation and increased the activities of antioxidant enzymes both in vivo and in vitro treated with excess iron. CUR can upregulate the level of FoxO1 and Nrf2, downregulate the level of p53 and the phosphorylation level of FoxO1, improve nuclear translocation of FoxO1, probably by inhibiting the IGFR/AKT signaling pathway, then increased cell viability and autophagy, and reduced apoptosis of MC3T3-E1 cells treated with excess iron by regulating the expression of FoxO1 target genes MnSOD, Gadd45a, Bim, FasL, and Rab7.

These results demonstrated that CUR was able to alleviate bone loss induced by oxidative stress resulting from iron overload, suggesting its potential use for the treatment of primary osteoporosis and bone loss in iron-overload-related diseases.

Copyright © 2019 Quanlong Zhang et al.


Curculigoside Protects against Excess-Iron-Induced Bone Loss by Attenuating Akt-FoxO1-Dependent Oxidative Damage to Mice and Osteoblastic MC3T3-E1 Cells.


Zhang Q1, Zhao L2, Shen Y3, He Y4, Cheng G1, Yin M5, Zhang Q1,4, Qin L1,4.

Publish date

2019 Dec 17

Description :

Curculigoside is the main saponin in C. orchioide, exerts significant antioxidant, anti-osteoporosis, antidepressant and neuroprotection effects. Curculigoside possesses significant anti-arthritic effects in vivo and in vitro via regulation of the JAK/STAT/NF-κB signaling pathway[1].