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Bufalin

$143

  • Brand : BIOFRON

  • Catalogue Number : BF-B2017

  • Specification : 98%

  • CAS number : 465-21-4

  • Formula : C24H34O4

  • Molecular Weight : 386.52

  • PUBCHEM ID : 9547215

  • Volume : 20mg

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Catalogue Number

BF-B2017

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

386.52

Appearance

White crystalline powder

Botanical Source

Bufo gargarizans

Structure Type

Others

Category

Standards;Natural Pytochemical;API

SMILES

CC12CCC(CC1CCC3C2CCC4(C3(CCC4C5=COC(=O)C=C5)O)C)O

Synonyms

3,14-dihydroxybufa-20,22-dienolide/(3β,5β)-3,14-Dihydroxybufa-20,22-dienolide/Bufalin: Bufa-20,22-dienolide, 3,14-dihydroxy-, (3b,5b)-,/Bufa-20,22-dienolide, 3,14-dihydroxy-, (3β,5β)-/5β-Bufa-20,22-dienolide, 3β,14-dihydroxy-/3β,14β-dihydroxy-5β-bufa-20,22-dienolide/(3b,5b)-3,14-Dihydroxybufa-20,22-dienolide/Bufalin

IUPAC Name

5-[(3S,5R,8R,9S,10S,13R,14S,17R)-3,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]pyran-2-one

Density

1.2±0.1 g/cm3

Solubility

Methanol

Flash Point

189.0±23.6 °C

Boiling Point

556.6±50.0 °C at 760 mmHg

Melting Point

242 - 243ºC

InChl

InChI=1S/C24H34O4/c1-22-10-7-17(25)13-16(22)4-5-20-19(22)8-11-23(2)18(9-12-24(20,23)27)15-3-6-21(26)28-14-15/h3,6,14,16-20,25,27H,4-5,7-13H2,1-2H3/t16-,17+,18-,19?,20?,22+,23-,24+/m1/s1

InChl Key

QEEBRPGZBVVINN-ZXRSHIDQSA-N

WGK Germany

RID/ADR

HS Code Reference

2937900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:465-21-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30150435

Abstract

Background/aim: Bufalin, bufadienolide present in Chan Su, has been shown to induce cancer cell apoptosis in many human cancer cells, including human leukemia cells, but its effects on immune responses are unknown.
Materials and methods: This study investigated whether bufalin affected immune responses of mice with WEHI-3 cell-generated leukemia in vivo. BALB/c mice were intraperitoneally injected with WEHI-3 cells to develop leukemia and then were treated with oral treatment with bufalin at different doses (0, 0.1, 0.2 and 0.4 mg/kg) for 2 weeks. At the end of treatment, all mice were weighted and blood was collected; liver and spleen tissues were collected for cell marker, phagocytosis, natural killer (NK) cell activity and T- and B-cell proliferation measurements by using flow cytometric assays.
Results: When compared with the leukemia control group, bufalin increased the body weight, but reduced liver and spleen weights, and reduced CD3, CD16 and Mac-3 cell markers at 0.4 mg/kg treatment and increased CD11b marker at 0.1 and 0.2 mg/kg treatment. Furthermore, bufalin at 0.4 mg/kg increased phagocytosis by macrophages isolated from peripheral blood mononuclear cells and at 0.1 mg/kg by those from the peritoneal cavity. Bufalin (0.2 and 0.4 mg/kg) increased NK cell cytotoxic activity at effector:target ratio of 50:1. Bufalin increased B-cell proliferation at 0.1 and 0.2 mg/kg treatment but only increased T-cell proliferation at 0.1 mg/kg. Bufalin increased glutamate oxaloacetate transaminase level at all dose treatments, increased glutamic pyruvic transaminase level only at 0.1 mg/kg treatment, but reduced the level of lactate dehydrogenase at all dose levels in mice with WEHI-3 cell-induced leukemia in vivo.
Conclusion: Bufalin increased immune responses by enhancing phagocytosis in mice with leukemia mice.

KEYWORDS

Bufalin; leukemia WEHI-3 cells; macrophage; natural killer cells; phagocytosis.

Title

Bufalin Enhances Immune Responses in Leukemic Mice Through Enhancing Phagocytosis of Macrophage In Vivo

Author

Yung-Luen Shih 1 2 3 , Jiann-Shang Chou 4 , Yung-Liang Chen 5 , Shu-Ching Hsueh 6 7 , Hsueh-Yu Chung 8 , Mei-Hui Lee 9 , Chao-Ping Chen 1 , Ming-Zhe Lee 10 , Hsin-Tu Hou 10 , Hsu-Feng Lu 10 , Kuo-Wei Chen 11 , Jing-Gung Chung 12 13

Publish date

Sep-Oct 2018

PMID

29636364

Abstract

The steroid receptor coactivator (SRC)-1 isoform/estrogen receptor (ER)-β axis has an essential role in endometriosis progression. In this context, therefore, bufalin was employed as a ‘tool compound’ to evaluate inhibitors of SRC in alternative endometriosis treatment. Bufalin effectively suppressed the growth of primary human endometrial stroma cells isolated from endometriosis patients compared to women without endometriosis and immortalized human endometrial epithelial and stromal cells expressing the SRC-1 isoform compared to their parental cells in vitroIn vivo, compared to the vehicle, bufalin treatment significantly suppressed the growth of endometriotic lesions in mice with surgically induced endometriosis because bufalin disrupted the functional axis of SRC-1 isoform/ERβ by increasing SRC-1 isoform protein stability, hyperactivating the transcriptional activity of the SRC-1 isoform and degrading the ERβ protein by proteasome 26S subunit, non-ATPase 2 in endometriotic lesions. Bufalin treatment elevated the apoptosis signaling in epithelial cells of endometriotic lesions. In stromal cells of endometriotic lesions, bufalin treatment increased the levels of pyroptosis markers (caspase 1 and the active form of interleukin 1β) and reduced proliferation. In addition, bufalin treatment increased the expression levels of endoplasmic reticulum-stress (ERS) markers (PKR-like ER kinase, protein disulfide isomerase and binding immunoglobulin) in endometriotic lesions. Collectively, the bufalin-induced disruption of the SRC-1 isoform/ERβ axis might induce apoptosis, pyroptosis and ERS signaling in endometriotic lesions, causing the suppression of endometriosis. Therefore, future generations of SRC-modulators could be employed as an alternative medical approach for endometriosis treatment.

KEYWORDS

Bufalin; leukemia WEHI-3 cells; macrophage; natural killer cells; phagocytosis.

Title

Bufalin Suppresses Endometriosis Progression by Inducing Pyroptosis and Apoptosis

Author

Yeon Jean Cho 1 2 , Jiyeun E Lee 1 , Mi Jin Park 1 , Bert W O'Malley 1 3 , Sang Jun Han 4 3

Publish date

2018 Jun

PMID

29653366

Abstract

Chansu is a traditional Chinese medicine that is generally recognized as a specific inhibitor of Na+/K+-ATPase. Bufalin, an active component of Chansu, is an endogenous steroid hormone with great potential as a cancer treatment. However, the mechanism by which it exerts its antitumor activity requires further research. Currently, the α1 subunit of Na+/K+-ATPase (ATP1A1) is known to exert important roles in tumorigenesis, and the precise mechanisms underlying the effect of Bufalin on the Na+/K+-ATPase α1 subunit was therefore investigated in this study to determine its role in glioblastoma treatments. The effect of ATP1A1 on the sensitivity of glioblastoma cells to Bufalin was investigated using MTT assays, RT-PCR and siRNA. Western blot was also used to explore the important roles of the ubiquitin-proteasome pathway in the Bufalin-mediated inhibition of ATP1A1. Xenografted mice were used to examine the anti-tumor activity of Bufalin in vivo. LC-MS/MS analysis was performed to determine the ability of Bufalin to traverse the blood-brain barrier (BBB). The results indicated that Bufalin inhibited the expression of ATP1A1 in glioblastoma by promoting the activation of proteasomes and the subsequent protein degradation of ATP1A1, while Bufalin had no effect on ATP1A1 protein synthesis. Bufalin also inhibited the expression of ATP1A1 in xenografted mice and significantly suppressed tumor growth. These data should contribute to future basic and clinical investigations of Bufalin. In conclusion, Bufalin significantly inhibited the expression of ATP1A1 in glioblastoma cells by activating the ubiquitin-proteasome signaling pathway. Bufalin may therefore have the potential to be an effective anti-glioma drug for human glioblastoma in the future.

KEYWORDS

Blood-Brain barrier; Bufalin; Glioblastoma multiforme; Proteasome; Sodium pump; Ubiquitin.

Title

Bufalin Inhibits Glioblastoma Growth by Promoting Proteasomal Degradation of the Na +/K +-ATPase α1 Subunit

Author

Yu-Long Lan 1 , Xun Wang 2 , Jia-Cheng Lou 2 , Jin-Shan Xing 2 , Zhen-Long Yu 3 , Hongjin Wang 4 , Shuang Zou 5 , Xiaochi Ma 6 , Bo Zhang 7

Publish date

2018 Jul 15


Description :

Bufalin a major digoxin-like immunoreactive component of the Chinese medicine Chan Su; has been shown to exert a potential for anticancer activity against various human cancer cell lines in vitro.IC50 value:Target: Anticaner natural compoundin vitro: bufalin remarkably inhibited growth in human gallbladder cancer cells by decreasing cell proliferation, inducing cell cycle arrest and apoptosis in a dose-dependent manner. Bufalin also disrupted the mitochondrial membrane potential (ΔΨm) and regulated the expression of cell cycle and apoptosis regulatory molecules. Activation of caspase-9 and the subsequent activation of caspase-3 indicated that bufalin may be inducing mitochondria apoptosis pathways [1]. bufalin suppressed the protein levels associated with DNA damage and repair, such as a DNA dependent serine/threonine protein kinase (DNA-PK), DNA repair proteins breast cancer 1, early onset (BRCA1), 14-3-3 σ (an important checkpoint keeper of DDR), mediator of DNA damage checkpoint 1 (MDC1), O6-ethylguanine-DNA methyltransferase (MGMT) and p53 (tumor suppressor protein) [2]. TNF-α significantly increased p65 translocation into nucleus (P < 0.01) and enhanced NF-κB DNA-binding activity, which were dose-dependently inhibited by bufalin. Furthermore, bufalin attenuated the TNF-α-induced interleukin-1beta (IL-1β), IL-6, and IL-8 production in RAFLSs in a concentration-dependent manner [3]. bufalin enhanced TRAIL-induced apoptosis in MCF-7 and MDA-MB-231 breast cancer cells by activating the extrinsic apoptotic pathway. Bufalin also promoted the clustering of death receptor 4 (DR4) and DR5 in aggregated lipid rafts [4].in vivo: bufalin (0.3 and 0.6 mg/kg, i.p.) potently decreased carrageenan-induced paw edema. Bufalin down regulated the expression levels of nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) during these treatments [5].