Escinmixture of saponins with anti-inflammatory, vasoconstrictor and vasoprotective effects CAS# 6805-41-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 6805-41-0 | SDF | Download SDF |
PubChem ID | 6433489 | Appearance | White powder |
Formula | C55H86O24 | M.Wt | 1131.3 |
Type of Compound | Isoprenoids | Storage | Desiccate at -20°C |
Synonyms | Aesculus;Aescin;66795-86-6 | ||
Solubility | Soluble in DMSO | ||
Chemical Name | (2S,3S,4S,5R,6R)-6-[[(4S,6bS,8R,9R)-9-acetyloxy-8-hydroxy-4,8a-bis(hydroxymethyl)-4,6a,6b,11,11,14b-hexamethyl-10-[(E)-2-methylbut-2-enoyl]oxy-1,2,3,4a,5,6,7,8,9,10,12,12a,14,14a-tetradecahydropicen-3-yl]oxy]-4-hydroxy-3-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-5-[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxane-2-carboxylic acid | ||
SMILES | CC=C(C)C(=O)OC1C(C2(C(CC1(C)C)C3=CCC4C5(CCC(C(C5CCC4(C3(CC2O)C)C)(C)CO)OC6C(C(C(C(O6)C(=O)O)OC7C(C(C(C(O7)CO)O)O)O)O)OC8C(C(C(C(O8)CO)O)O)O)C)CO)OC(=O)C | ||
Standard InChIKey | AXNVHPCVMSNXNP-YSYFQUGBSA-N | ||
Standard InChI | InChI=1S/C55H86O24/c1-10-23(2)46(71)79-43-44(72-24(3)60)55(22-59)26(17-50(43,4)5)25-11-12-30-51(6)15-14-32(52(7,21-58)29(51)13-16-53(30,8)54(25,9)18-31(55)61)75-49-41(77-48-38(67)36(65)34(63)28(20-57)74-48)39(68)40(42(78-49)45(69)70)76-47-37(66)35(64)33(62)27(19-56)73-47/h10-11,26-44,47-49,56-59,61-68H,12-22H2,1-9H3,(H,69,70)/b23-10+/t26?,27-,28-,29?,30?,31-,32?,33-,34-,35+,36+,37-,38-,39+,40+,41-,42+,43?,44+,47+,48-,49-,51?,52-,53?,54-,55?/m1/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Escin Dilution Calculator
Escin Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 0.8839 mL | 4.4197 mL | 8.8394 mL | 17.6788 mL | 22.0985 mL |
5 mM | 0.1768 mL | 0.8839 mL | 1.7679 mL | 3.5358 mL | 4.4197 mL |
10 mM | 0.0884 mL | 0.442 mL | 0.8839 mL | 1.7679 mL | 2.2098 mL |
50 mM | 0.0177 mL | 0.0884 mL | 0.1768 mL | 0.3536 mL | 0.442 mL |
100 mM | 0.0088 mL | 0.0442 mL | 0.0884 mL | 0.1768 mL | 0.221 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Evaluation of the effect of polyphenol of escin compared with ibuprofen and dexamethasone in synoviocyte model for osteoarthritis: an in vitro study.[Pubmed:29663159]
Clin Rheumatol. 2018 Sep;37(9):2471-2478.
Osteoarthritis (OA) is a chronic degenerative joint disease with inflammatory component. It is associated with progressive histological alterations and disabling symptoms. Today, drugs such as glucocorticoids (GCs) and nonsteroidal anti-inflammatory drugs (NSIADs) are commonly employed for treatment of osteoarthritis, but have serious and life-threatening side effects. The aim of the current study is to evaluate the effects of Escin on cyclooxygenase-2 (COX-2, isoform), inducible nitric oxide synthase (iNOS), interleukin-1beta (IL-1beta), interleukin-18 (IL-18), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) (1), as well as prostaglandin E2 (PGE2) on inflammatory cells, similar osteoarthritis in synoviocytes, and monocytes/macrophages, and to compare it with dexamethasone (DEX) and ibuprofen (IBP). Synovial cells were isolated from synovial membrane of the radiocarpal joint cartilage of an 8-month-old Holstein cow. THP-1 cells were prepared from Pasteur Institute of Iran. Cells were cultivated and exposed to lipopolysaccharide (LPS) stimulation without, or in the presence of, DEX, IBP, or Escin. The gene expressions of IL-1beta, TNF-alpha, IL-18, COX-2, and iNOS were evaluated by real-time PCR. Concentrations of NO and PGE2 were measured by ELISA methods. Our cells secreted an increased amounts of IL-1beta, TNF-alpha, IL-18, COX-2, iNOS, NO, and PGE2 in response to LPS stimulation in all conditions. Escin can quench the gene expression of COX-2, iNOS, IL-1beta, IL-18, and TNF-alpha in synoviocyte cells and production of NO and PGE2 in monocyte/macrophage cells alike DEX and IBP. We can use from Escin for the treatment of osteoarthritis as an anti-inflammatory agent in the latter but further studies to support the results from such a model are needed.
beta-Escin Effectively Modulates HUVECS Proliferation and Tube Formation.[Pubmed:29342121]
Molecules. 2018 Jan 17;23(1). pii: molecules23010197.
In the present study we evaluated the anti-angiogenic activities of beta-Escin (the major active compound of Aesculus hippocastanum L. seeds). Human umbilical-vein endothelial cells (HUVECs) were used as an in vitro model for studying the molecular mechanism underlying the anti-angiogenic effect of beta-Escin. We investigated the in vitro effects on proliferation, migration, and tube formation of HUVECs and in vivo anti-angiogenic activity was evaluated in a chick chorioallantoic membrane (CAM) angiogenesis assay. Moreover, the effect on gene expressions was determined by the RT2 ProfilerTM human angiogenesis PCR Array. It was found that beta-Escin exerts inhibitory effect on the basic fibroblast growth factor (bFGF)-induced proliferation, migration and tube formation, as well as CAM angiogenesis in vivo. The inhibition of critical steps of angiogenic process observed with beta-Escin could be partially explained by suppression of Akt activation in response to bFGF. Moreover, the anti-angiogenic effects of beta-Escin could also be mediated via inhibition of EFNB2 and FGF-1 gene expressions in endothelial cells. In conclusion, beta-Escin affects endothelial cells as a negative mediator of angiogenesis in vitro and in vivo and may therefore be considered as a promising candidate for further research elucidating its underlying mechanism of action.
Novel Colloidal Microstructures of beta-Escin and the Liposomal Components Cholesterol and DPPC.[Pubmed:29797304]
Planta Med. 2018 Nov;84(16):1219-1227.
The discovery of immunostimulating complex formation by the saponin Quil A from the plant Quillaja saponaria with cholesterol and a phospholipid opened up new avenues for the development of drug delivery systems for vaccine application with additional adjuvant properties. In this study, beta-Escin, a monodesmosidic triterpene saponin from horse chestnut, was investigated in terms of its interaction with liposomal components (cholesterol, dipalmitoylphosphatidylcholine) by Langmuir film balance studies and with regard to particle formation visualized by transmission electron microscopy. A strong interaction of beta-Escin with cholesterol was observed by Langmuir isotherms due to the intercalation of the saponin into the monolayer, whereas no interaction occurred with dipalmitoylphosphatidylcholine. Transmission electron microscopy studies also confirmed the strong interaction of beta-Escin with cholesterol. In aqueous pseudo-ternary systems (beta-Escin, dipalmitoylphosphatidylcholine, cholesterol) and in pseudo-binary systems (beta-Escin, cholesterol), new colloidal structures built up from ring-like and worm-like subunits were observed with a size of about 100 - 200 nm. These colloidal structures are formed in pseudo-binary systems by aggregation of the subunits, whereas in pseudo-ternary systems, they are formed among others by attacking the liposomal membrane. The rehydration of the liposomal dispersions in NANOpure water or Tris buffer pH 7.4 (140 mM) resulted in the same particle formation. In contrast, the sequence of the dispersions' production process affected the particle formation. Unless adding the saponin to the other components from the beginning, just a liposomal dispersion was formed without any colloidal aggregates of the subunits mentioned above.
Escin-induced DNA damage promotes escin-induced apoptosis in human colorectal cancer cells via p62 regulation of the ATM/gammaH2AX pathway.[Pubmed:29849127]
Acta Pharmacol Sin. 2018 Oct;39(10):1645-1660.
Escin, a triterpene saponin isolated from horse chestnut seed, has been used to treat encephaledema, tissue swelling and chronic venous insufficiency. Recent studies show that Escin induces cell cycle arrest, tumor proliferation inhibition and tumor cell apoptosis. But the relationship between Escin-induced DNA damage and cell apoptosis in tumor cells remains unclear. In this study, we investigated whether and how Escin-induced DNA damage contributed to Escin-induced apoptosis in human colorectal cancer cells. Escin (5-80 mug/mL) dose-dependently inhibited the cell viability and colony formation in HCT116 and HCT8 cells. Escin treatment induced DNA damage, leading to p-ATM and gammaH2AX upregulation. Meanwhile, Escin treatment increased the expression of p62, an adaptor protein, which played a crucial role in controlling cell survival and tumorigenesis, and had a protective effect against Escin-induced DNA damage: knockdown of p62 apparently enhanced Escin-induced DNA damage, whereas overexpression of p62 reduced Escin-induced DNA damage. In addition, Escin treatment induced concentration- and time-dependent apoptosis. Similarly, knockdown of p62 significantly increased Escin-induced apoptosis in vitro and produced en Escin-like antitumor effect in vivo. Overexpression of p62 decreased the rate of apoptosis. Further studies revealed that the functions of p62 in Escin-induced DNA damage were associated with Escin-induced apoptosis, and p62 knockdown combined with the ATM inhibitor KU55933 augmented Escin-induced DNA damage and further increased Escin-induced apoptosis. In conclusion, our results demonstrate that p62 regulates ATM/gammaH2AX pathway-mediated Escin-induced DNA damage and apoptosis.
Anti-inflammatory effect of external use of escin on cutaneous inflammation: possible involvement of glucocorticoids receptor.[Pubmed:29455725]
Chin J Nat Med. 2018 Feb;16(2):105-112.
Escin, as an internally applied anti-inflammatory agent, has been widely used in the treatment of inflammation and edema resulting from trauma or operation in the clinic. However, the effect of its external use on cutaneous inflammation and edema remains unexplored. In the present study, the anti-inflammatory and anti-edematous effects of external use of Escin were studied in carrageenan-induced paw edema and histamine-induced capillary permeability in rats, paraxylene-induced ear swelling in mice, and cotton pellet-induced granuloma in rats. Effects of external use of Escin gel on prostaglandin E2 (PGE2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) were determined by ELISA. The anti-inflammatory mechanism was explored by detecting the expression of glucocorticoid receptor (GR) with Western blotting and Real-time PCR analyses, with further exploration of nuclear factor-kappaB (NF-kappaB), p38 mitogen-activated protein kinase (P38MAPK) and activator protein-1 (AP-1) expressions. We demonstrated that external use of Escin showed significant anti-inflammatory effects on acute and chronic inflammation in different animal models and its anti-inflammatory effects might be related to down-regulation of PGE2, TNF-alpha, and IL-1beta. The results also showed that Escin exerted its anti-inflammatory effects by promoting the expression of GR, with the possible mechanism being inhibition of the expressions of GR-related signaling molecules such as NF-kappaB and AP-1.
Molecular targets and anti-cancer potential of escin.[Pubmed:29474858]
Cancer Lett. 2018 May 28;422:1-8.
Escin is a mixture of triterpenoid saponins extracted from the horse chestnut tree, Aesculus hippocastanum. Its potent anti-inflammatory and anti-odematous properties makes it a choice of therapy against chronic venous insufficiency and odema. More recently, Escin is being actively investigated for its potential activity against diverse cancers. It exhibits anti-cancer effects in many cancer cell models including lung adenocarcinoma, hepatocellular carcinoma and leukemia. Escin also attenuates tumor growth and metastases in various in vivo models. Importantly, Escin augments the effects of existing chemotherapeutic drugs, thereby supporting the role of Escin as an adjunct or alternative anti-cancer therapy. The beneficial effects of Escin can be attributed to its inhibition of proliferation and induction of cell cycle arrest. By regulating transcription factors/growth factors mediated oncogenic pathways, Escin also potentially mitigates chronic inflammatory processes that are linked to cancer survival and resistance. This review provides a comprehensive overview of the current knowledge of Escin and its potential as an anti-cancer therapy through its anti-proliferative, pro-apoptotic, and anti-inflammatory effects.