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Aucubin

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-A3028

  • Specification : 98%

  • CAS number : 479-98-1

  • Formula : C15H22O9

  • Molecular Weight : 346.33

  • PUBCHEM ID : 91458

  • Volume : 25mg

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Catalogue Number

BF-A3028

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

346.33

Appearance

White crystalline powder

Botanical Source

Aucuba chinensis

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=COC(C2C1C(C=C2CO)O)OC3C(C(C(C(O3)CO)O)O)O

Synonyms

Rhimanthin/Aucubin/Rhinanthin/(2S,3R,4S,5S,6R)-2-{[(1S,4aR,5S,7aS)-5-Hydroxy-7-(hydroxymethyl)-1,4a,5,7a-tetrahydrocyclopenta[c]pyran-1-yl]oxy}-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol/Rhimantin/(1S,4aR,5S,7aS)-5-Hydroxy-7-(hydroxymethyl)-1,4a,5,7a-tetrahydrocyclopenta[c]pyran-1-yl β-D-glucopyranoside/β-D-Glucopyranoside, (1S,4aR,5S,7aS)-1,4a,5,7a-tetrahydro-5-hydroxy-7-(hydroxymethyl)cyclopenta[c]pyran-1-yl/AUCUBOSIDE/[1S-(1a,4aa,5a,7a)]-1,4a,5,7a-Tetrahydro-5-hydroxy-7-(hydroxymethyl)cyclopenta[c]pyran-1-yl-b-D-glucopyranoside/(2S,3R,4S,5S,6R)-2-{[(1S,4aR,5S,7aS)-5-Hydroxy-7-(hydroxymethyl)-1,4a,5,7a-tetrahydrocyclopenta[c]pyran-1-yl]oxy}-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol/(2S,3R,4S,5S,6R)-2-{[(1S,4aR,5S,7aS)-5-Hydroxy-7-(hydroxymethyl)-1,4a,5,7a-tetrahydrocyclopenta[c]pyr-1-yl]oxy}-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol/(1S,4aR,5S,7aS)-5-Hydroxy-7-(hydroxymethyl)-1,4a,5,7a-tetrahydrocyclopenta[c]pyr-1-yl-β-D-glucopyranoside

IUPAC Name

(2S,3R,4S,5S,6R)-2-[[(1S,4aR,5S,7aS)-5-hydroxy-7-(hydroxymethyl)-1,4a,5,7a-tetrahydrocyclopenta[c]pyran-1-yl]oxy]-6-(hydroxymethyl)oxane-3,4,5-triol

Density

1.6±0.1 g/cm3

Solubility

Flash Point

358.4±31.5 °C

Boiling Point

669.0±55.0 °C at 760 mmHg

Melting Point

180 - 184ºC

InChl

InChl Key

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#:479-98-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28785877

Abstract

Pulmonary fibrosis is a life-threatening disease characterized by progressive dyspnea and worsening of pulmonary function. No effective therapeutic strategy for pulmonary fibrosis has been established. Aucubin is a natural constituent with a monoterpene cyclic ring system. The potency of aucubin in protecting cellular components against inflammation, oxidative stress, and proliferation effects is well documented. In this study, we investigated the protective effect of aucubin against pulmonary fibrosis in mice. A mouse model of pulmonary fibrosis was established by intratracheal injection of bleomycin (BLM), and aucubin was administered for 21 days after BLM injection. We found that aucubin decreased the breathing frequency and increased the lung dynamic compliance of BLM-stimulated mice detected by Buxco pulmonary function testing system. Histological examination showed that aucubin alleviated BLM-induced lung parenchymal fibrotic changes. Aucubin also reduced the intrapulmonary collagen disposition and inflammatory injury induced by BLM. In addition, aucubin reduced the expression of pro-fibrotic protein transforming growth factor (TGF)-β1 and α-smooth muscle actin (α-SMA) of pulmonary fibrosis mice induced by BLM. Furthermore, the effect of aucubin on the proliferation and differentiation of fibroblast was investigated in vitro. Aucubin inhibited the mRNA and protein expression of Ki67 and proliferating cell nuclear antigen (PCNA) induced by TGF-β1 and reduced the cell proliferation in a murine fibroblast cell NIH3T3. Aucubin also reduced the collagen syntheses and α-SMA expression induced by TGF-β1 in fibroblast. Our results indicate that aucubin inhibits inflammation, fibroblast proliferation, and differentiation, exerting protective effects against BLM-induced pulmonary fibrosis in a mouse model. This study provides an evidence that aucubin may be a novel drug for pulmonary fibrosis.

KEYWORDS

aucubin; bleomycin; fibroblast; pulmonary fibrosis; transform growth factor-β1

Title

Aucubin Alleviates Bleomycin-Induced Pulmonary Fibrosis in a Mouse Model.

Author

Zhou Y1, Li P1, Duan JX2, Liu T1, Guan XX1, Mei WX1, Liu YP1, Sun GY1, Wan L1, Zhong WJ1, Ouyang DS3, Guan CX4.

Publish date

2017 Dec

PMID

30046377

Abstract

Whether aucubin could protect myocardial infarction- (MI-) induced cardiac remodeling is not clear. In this study, in a mouse model, cardiac remodeling was induced by left anterior descending coronary artery ligation surgery. Mice were intraperitoneally injected with aucubin (10 mg/kg) 3 days post-MI. Two weeks post-MI, mice in the aucubin treatment group showed decreased mortality, decreased infarct size, and improved cardiac function. Aucubin also decreased cardiac remodeling post-MI. Consistently, aucubin protected cardiomyocytes against hypoxic injury in vitro. Mechanistically, we found that aucubin inhibited the ASK1/JNK signaling. These effects were abolished by the JNK activator. Moreover, we found that the oxidative stress was attenuated in both in vivo aucubin-treated mice heart and in vitro-treated cardiomyocytes, which caused decreased thioredoxin (Trx) consumption, leading to ASK1 forming the inactive complex with Trx. Aucubin increased nNOS-derived NO production in vivo and vitro. The protective effects of aucubin were reversed by the NOS inhibitors L-NAME and L-VINO in vitro. Furthermore, nNOS knockout mice also reversed the protective effects of aucubin on cardiac remodeling. Taken together, aucubin protects against cardiac remodeling post-MI through activation of the nNOS/NO pathway, which subsequently attenuates the ROS production, increases Trx preservation, and leads to inhibition of the ASK1/JNK pathway.

Title

Aucubin Protects against Myocardial Infarction-Induced Cardiac Remodeling via nNOS/NO-Regulated Oxidative Stress.

Author

Yang Z1,2,3, Wu QQ1,2,3, Xiao Y1,2,3, Duan MX1,2,3, Liu C1,2,3, Yuan Y1,2,3, Meng YY1,2,3, Liao HH1,2,3, Tang QZ1,2,3.

Publish date

2018 Jun 25

PMID

31631977

Abstract

Objective:
Chondrocyte apoptosis has also been strongly correlated with the severity of cartilage damage and matrix depletion in an osteoarthritis (OA) joint. Therefore, pharmacological inhibitors of apoptosis may provide a novel treatment option for patients with OA. Aucubin, a natural compound isolated from Eucommia ulmoides, has been proved to possess antioxidative and anti-apoptotic properties. However, anti-osteoarthritis effect of aucubin in animal model and anti-apoptotic response of aucubin in OA chondrocytes remain unclear. This study aimed to determine whether aucubin could slow progression of OA in a mouse model and inhibit the IL-1β-induced chondrocyte apoptosis.
Methods:
OA severity and articular cartilage degradation were evaluated by Safranin-O staining, Hematoxylin-eosin (H&E) staining, and Osteoarthritis Research Society International (OARSI) standards. Chondrocyte viability was observed by Cell Counting Kit-8 (CCK8) and live/dead cells assay; the apoptotic rate of chondrocytes was evaluated by flow cytometry (FCM) with Annexin V-FITC/PI kit. Mediators of apoptosis were tested by Western blot of Bax, caspase-3, caspase-9, and Bcl-2 expression. The intracellular levels of Reactive oxygen species (ROS) were assessed by the probe of 2,7-Dichlorofluorescin diacetate (DCFH-DA).
Results:
The articular cartilage in the limb with destabilization of the medial meniscus (DMM) exhibited early OA-like manifestations characterized by proteoglycan loss, cartilage fibrillation, and erosion, with lower OARSI score. Oral administration of aucubin remarkably attenuated the loss of proteoglycan and the articular cartilage erosion and decreased the OARSI scores underwent DMM surgery. Aucubin treatment significantly reverses IL-1β-induced cytotoxicity and attenuated the IL-1β-induced chondrocyte apoptosis. In addition, aucubin can significantly inhibit mediators of apoptosis in rat primary chondrocytes. Furthermore, aucubin remarkably attenuated the IL-1β-induced intracellular ROS production.
Conclusion:
Our findings suggest that aucubin has a protective effect on articular cartilage and slowing progression of OA in a mouse model. This protective effect may result from inhibiting chondrocyte apoptosis and excessive ROS production.
© 2019 Wang et al.

KEYWORDS

IL-1β; ROS; apoptosis; aucubin; osteoarthritis

Title

Aucubin Protects Chondrocytes Against IL-1β-Induced Apoptosis In Vitro And Inhibits Osteoarthritis In Mice Model.

Author

Wang BW#1, Jiang Y#1, Yao ZL#1, Chen PS2, Yu B#1, Wang SN1.

Publish date

2019 Oct 9


Description :

Aucubin is an iridoid glycoside with a wide range of biological activities, including anti-inflammatory, anti-microbial, anti-algesic as well as anti-tumor activities.IC50 value:Target:In vitro: Aucubin promotes neuronal differentiation and neurite outgrowth in neural stem cells cultured primarily from the rat embryonic hippocampus [1]. Aucubin significantly reversed the elevated gene and protein expression of MMP-3, MMP-9, MMP-13, iNOS, COX-2 and the production of NO induced by IL-1β challenge in rat chondrocytes [2]. In vivo: