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Aloe-emodin

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-A1005

  • Specification : 98%

  • CAS number : 481-72-1

  • Formula : C15H10O5

  • Molecular Weight : 270.24

  • PUBCHEM ID : 10207

  • Volume : 20mg

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Catalogue Number

BF-A1005

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

270.24

Appearance

Orange crystalline powder

Botanical Source

Xanthium sibiricum,Aloe vera,Rheum palmatum,Reynoutria japonica,Eremurus anisopterus

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC2=C(C(=C1)O)C(=O)C3=C(C2=O)C=C(C=C3O)CO

Synonyms

Aloe emodin/1,8-Dihydroxy-3-(hydroxymethyl)anthracen-9,10-dion/1,8-Dihydroxy-3-(hydroxymethyl)anthraquinone/ALOE-EMODIN/Aloeemodin:9,10-Anthracenedione,1,8-dihydroxy-3-(hydroxymethyl)-,/Aloeemodin/1,8-Dihydroxy-3-(hydroxymethyl)anthraquinone,3-Hydroxymethylchrysazine,Aloe-emodin/3-Hydroxymethylchrysazine/EMODINE/1,8-dihydroxy-3-(hydroxymethyl)anthracene-9,10-dione/Rhabarberone/1,8-Dihydroxy-3-(hydroxymethyl)anthra-9,10-quinone/3-Hydroxymethylchrysazin/1,8-Dihydroxy-3-(hydroxymethyl)anthraquinone,3-Hydroxymethylchrysazine/1,8-Dihydroxy-3-(hydroxymethyl)-9,10-anthraquinone/Diacerein impurity B/9,10-Anthracenedione, 1,8-dihydroxy-3-(hydroxymethyl)-

IUPAC Name

1,8-dihydroxy-3-(hydroxymethyl)anthracene-9,10-dione

Density

1.6±0.1 g/cm3

Solubility

Methanol; Ethyl Acetate; DMF

Flash Point

311.9±26.6 °C

Boiling Point

568.8±50.0 °C at 760 mmHg

Melting Point

223-224°C

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2914690000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:481-72-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30199885

Abstract

BACKGROUND Recently, colorectal cancer has become a more common type of tumor in the world. Research has reported that several kinds of single compounds of Chinese herbs have shown anti-tumor activity in colorectal cancer. Aloe-emodin (AE), a natural compound extract from Aloe Vera, has been discovered to suppress cell proliferation and accelerate apoptosis in a variety of tumor cells. Whether AE exerts an effect on colorectal cancer cells has not yet been investigated. MATERIAL AND METHODS In this study, we examined the impact of AE on SW620 and HT29 colorectal cancer cell lines. After treatment with various concentrations of AE (10, 20, and 40 μM), cell proliferation, cell apoptosis, reactive oxygen species (ROS) generation, cytosolic calcium level, and related gene expression were analyzed. RESULTS Our results indicated that AE suppressed cell viability and induced cell apoptosis in SW620 and HT29 cell lines. Furthermore, both cell lines when exposed to AE generated ROS, which induces endoplasmic reticulum (ER) stress. We then detected the expression of ER stress-related proteins and cytosolic calcium levels. We found that cells exposure to AE had upregulation of unfolded protein response (UPR) proteins like glucose-related protein 78 (GRP78), phosphorylated protein kinase R (PKR)-like ER kinase (p-PERK), phosphorylated eukaryotic initiation factor-2α (p-eIF2α), and transcription factor C/EBP homologous protein (CHOP). Meanwhile, we detected an increased cytosolic calcium content followed by the upregulation of the calpain-1, calpain-2 and caspase-12. CHOP and caspase-12 are important regulatory factors leading to cell apoptosis. CONCLUSIONS AE might serve as a candidate in the treatment of colorectal cancer through inducing ER stress-dependent apoptosis.

Title

Aloe-Emodin Induces Endoplasmic Reticulum Stress-Dependent Apoptosis in Colorectal Cancer Cells.

Author

Cheng C1, Dong W1.

Publish date

2018 Sep 10

PMID

30672276

Abstract

Aloe-emodin (AE), an anthraquinone derivative, is a bioactive ingredient isolated from rhubarb which is used to treat inflammatory illnesses in China and many other countries in Asia. AE has shown a wide range of pharmacological effects. Recent studies showed that exposure to AE could cause DNA damage and cytotoxicity. The goals of the present study are aimed at (1) exploration of oxidative metabolism pathways of AE, (2) identification of P450 enzymes which respond the hydroxylation of AE, and (3) determination of electrophilicity of AE and its oxidative metabolites. Two hydroxylation metabolites (M1 and M2) and four GSH conjugates (M3-M6) were found in incubations consisting of AE, rat or human liver microsomes, and NADPH supplemented with GSH. Conjugates M3 and M4 came from AE itself, and M5 and M6 originated from M1 and M2 individually. M1 and M2 (5-hydroxy aloe-emodin) and M3-M6 were also detected in rat primary hepatocytes after exposure to AE. Additionally, biliary M3, M4, and M6 were detected in rats given AE. Urinary M1, M2, and M7 (a NAC conjugate) were observed in animals administered AE. Recombinant P450 enzyme incubations illustrated that hydroxylation of AE was primarily catalyzed by P450 1A2, 3A4, and 3A5. The metabolism investigation will help us to better understand the biochemical mechanisms of cytotoxicity induced by AE.

Title

Chemical Reactivity of Aloe-Emodin and Its Hydroxylation Metabolites to Thiols.

Author

Wang X1, Xin X1, Sun Y1, Zou L1, Li H1, Zhao Y1, Li R1, Peng Y1, Zheng J1,2.

Publish date

2019 Feb 18

PMID

24707862

Abstract

Aloe-emodin (AE), a bioactive anthraquinone derived from both Aloe vera and Rheum officinale, has recently been demonstrated to have various pharmacological activities. With the widespread popularity of natural products, such as antineoplastic drugs, AE has attracted much attention due to its remarkable antineoplastic activity on multiple tumor cells involving multi-channel mechanisms, including the disruption of cell cycle, induction of apoptosis, anti-metastasis, antiangiogenic, and strengthening of immune function. Experimental data have revealed AE as a potentially potent anti-cancer candidate. Despite this, the pharmaceutical application of AE is still in a fledging period as most research has concentrated on the elucidation of the molecular mechanism of action of existing treatments, rather than the development of novel formulations. Therefore, the present review summarizes the potential toxicity, molecular mechanism, pharmacokinetic characteristics, and pharmaceutical development of AE as an antineoplastic agent. This is based on its physicochemical properties, in an attempt to encourage further research on AE as a potential anti-cancer agent.

Title

Potential antineoplastic effects of Aloe-emodin: a comprehensive review.

Author

Chen R1, Zhang J, Hu Y, Wang S, Chen M, Wang Y.

Publish date

2014


Description :

Aloe emodin is a hydroxyanthraquinone present in Aloe vera leaves, has a specific in vitro and in vivo antitumor activity.IC50 value:Target:in vitro: aloe-emodin treatment led to the dissociation of heat shock protein 90 (HSP90) and ER α and increased ER α ubiquitination. Protein fractionation results suggest that aloe-emodin tended to induce cytosolic ER α degradation [1]. Aloe-emodin, a natural compound found in aloe, inhibited both proliferation and anchorage-independent growth of PC3 cells. Protein content analysis suggested that activation of the downstream substrates of mTORC2, Akt and PKCα, was inhibited by aloe-emodin treatment. Pull-down assay and in vitro kinase assay results indicated that aloe-emodin could bind with mTORC2 in cells and inhibit its kinase activity [2]. Of three anthraquinone derivatives, aloe-emodin, with a lower cytotoxicity showed concentration-dependently reducing virus-induced cytopathic effect and inhibiting replication of influenza A in MDCK cells. Galectin-3 also inhibited influenza A virus replication. Proteomic analysis of treated cells indicated galectin-3 up-regulation as one anti-influenza A virus action by aloe-emodin. Since galectin-3 exhibited cytokine-like regulatory actions via JAK/STAT pathways, aloe-emodin also restored NS1-inhibited STAT1-mediated antiviral responses in transfected cells: e.g., STAT1 phosphorylation of interferon (IFN) stimulation response element (ISRE)-driven promoter, RNA-dependent protein kinase (PKR) and 2'5',-oligoadenylate synthetase (2'5',-OAS) expression [3]. AE downregulated mRNA expression and promoter/gelatinolytic activity of Matrix Metalloproteinase (MMP)-2/9, as well as the RhoB expression at gene and protein level. AE suppressed the nuclear translocation and DNA binding of NF-κB [4].in vivo: Aloe-emodin also exhibited tumor suppression effects in vivo in an athymic nude mouse model [2].