Corilagin

Corilagin
Product Name Corilagin
CAS No.: 23094-69-1
Catalog No.: CFN90176
Molecular Formula: C27H22O18
Molecular Weight: 634.45 g/mol
Purity: >=98%
Type of Compound: Phenols
Physical Desc.: Powder
Targets: TLR | TGF-β/Smad | LDL | HO-1 | HSV | IL Receptor | p65 | NF-kB | IkB | TNF-α | Akt | p53 | p21 | Caspase | Adrenergic Receptor | IKK
Source: The herbs of Geranium wilfordii Maxim.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $100/20mg
Corilagin has antitumour, anti-inflammatory, antioxidant, antifibrotics, antiviral, antibacterial, hepatoprotective, antiatherogenic, and antihypertensive activities. Corilagin reduces the cytotoxicity induced by EV71 or CA16 on Vero cells with and IC50 value of 5.6 and 32.33 μg/mL, respectively; it shows the potential to protect against HSV-1-induced encephalitis, and the beneficial effects may be mediated by inhibiting TLR2 signaling pathways. Corilagin attenuates bleomycin-induced epithelial injury and fibrosis via inactivation of oxidative stress, proinflammatory cytokine release and NF-κB and TGF-β1 signaling; it suppresses the activity of beta-lactamase to some extent.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Phytother Res. 2014 May;28(5):781-3.
    Sensitization of Hep3B hepatoma cells to cisplatin and doxorubicin by corilagin.[Pubmed: 23913631]
    The anticancer action of gallotannins is a well-developed topic. We have demonstrated the in vivo antitumour activity of Corilagin on Hep3B hepatoma using the xenograft athymic nude mice model.
    METHODS AND RESULTS:
    Here, we further report the potential sensitization of Hep3B hepatoma cells to cisplatin and doxorubicin by Corilagin. Our results showed that Corilagin is able to enhance the cytotoxicity of both cisplatin and doxorubicin on the Hep3B hepatoma cells.
    CONCLUSIONS:
    We speculate the possible use of Corilagin in combination with low dosages of the anticancer chemotherapeutic standard drugs like cisplatin and doxorubicin, with the aim of obtaining an increment in the anticancer effect.
    Arch Pharm Res. 2015 Feb;38(2):193-202.
    Antiviral effects of Phyllanthus urinaria containing corilagin against human enterovirus 71 and Coxsackievirus A16 in vitro.[Pubmed: 24752860]
    Human enterovirus 71 (EV71) and Coxsackievirus A16 (CA16) are major causative agents of hand, foot, and mouth disease (HFMD) especially in infants and children under 5 years of age. Despite recent outbreaks of HFMD, there are no approved therapeutics against EV71 and CA16 infection. Moreover, in a small percentage of cases, the disease progression can lead to serious complications of the central nervous system.
    METHODS AND RESULTS:
    In this study, we investigated the antiviral effect of Corilagin and Phyllanthus urinaria extract, which contains Corilagin as a major component, on EV71 and CA16 infection in vitro. Our results indicate that Corilagin reduces the cytotoxicity induced by EV71 or CA16 on Vero cells with and IC50 value of 5.6 and 32.33 μg/mL, respectively. We confirmed the presence of Corilagin in EtOAc and BuOH fractions from P. urinaria extract and this correlated with antiviral activity of the fractions against EV71 or CA16. Future studies will be required to confirm the antiviral activity of Corilagin and P. urinaria extract in vivo. Challenging a model with a lethal dose of viral infection will be required to test this.
    CONCLUSIONS:
    Collectively, our work provides potential candidates for the development of novel drugs to treat HFMD.
    Microbiol Immunol. 2004;48(1):67-73.
    Mechanisms of action of corilagin and tellimagrandin I that remarkably potentiate the activity of beta-lactams against methicillin-resistant Staphylococcus aureus.[Pubmed: 14734860]
    Corilagin and tellimagrandin I are polyphenols isolated from the extract of Arctostaphylos uvaursi and Rosa canina L. (rose red), respectively. We have reported that Corilagin and tellimagrandin I remarkably reduced the minimum inhibitory concentration (MIC) of beta-lactams in methicillin-resistant Staphylococcus aureus(MRSA).
    METHODS AND RESULTS:
    In this study, we investigated the effect of Corilagin and tellimagrandin I on the penicillin binding protein 2 '(2a) (PBP2 '(PBP2a)) which mainly confers the resistance to beta-lactam antibiotics in MRSA. These compounds when added to the culture medium were found to decrease production of the PBP2 '(PBP2a) slightly. Using BOCILLIN FL, a fluorescent-labeled benzyl penicillin, we found that PBP2 '(PBP2a) in MRSA cells that were grown in medium containing Corilagin or tellimagrandin I almost completely lost the ability to bind BOCILLIN FL. The binding activity of PBP2 and PBP3 were also reduced to some extent by these compounds.
    CONCLUSIONS:
    These results indicate that inactivation of PBPs, especially of PBP2 '(PBP2a), by Corilagin or tellimagrandin I is the major reason for the remarkable reduction in the resistance level of beta-lactams in MRSA. Corilagin or tellimagrandin I suppressed the activity of beta-lactamase to some extent.
    Int J Mol Sci. 2014 May 30;15(6):9762-79.
    Corilagin attenuates aerosol bleomycin-induced experimental lung injury.[Pubmed: 24886817]
    Idiopathic pulmonary fibrosis (IPF) is a progressing lethal disease with few clinically effective therapies. Corilagin is a tannin derivative which shows anti-inflammatory and antifibrotics properties and is potentiated in treating IPF.
    METHODS AND RESULTS:
    Here, we investigated the effect of Corilagin on lung injury following bleomycin exposure in an animal model of pulmonary fibrosis. Corilagin abrogated bleomycin-induced lung fibrosis as assessed by H&E; Masson's trichrome staining and lung hydroxyproline content in lung tissue. Corilagin reduced the number of apoptotic lung cells and prevented lung epithelial cells from membrane breakdown, effluence of lamellar bodies and thickening of the respiratory membrane. Bleomycin exposure induced expression of MDA, IKKα, phosphorylated IKKα (p-IKKα), NF-κB P65, TNF-α and IL-1β, and reduced I-κB expression in mice lung tissue or in BALF. These changes were reversed by high-dose Corilagin (100 mg/kg i.p) more dramatically than by low dose (10 mg/kg i.p). Last, Corilagin inhibits TGF-β1 production and α-SMA expression in lung tissue samples.
    CONCLUSIONS:
    Taken together, these findings confirmed that Corilagin attenuates bleomycin-induced epithelial injury and fibrosis via inactivation of oxidative stress, proinflammatory cytokine release and NF-κB and TGF-β1 signaling. Corilagin may serve as a promising therapeutic agent for pulmonary fibrosis.
    Phytomedicine. 2007 Nov;14(11):755-62.
    Antioxidant and hepatoprotective actions of medicinal herb, Terminalia catappa L. from Okinawa Island and its tannin corilagin.[Pubmed: 17293097 ]
    The antioxidant and hepatoprotective actions of Terminalia catappa L. collected from Okinawa Island were evaluated in vitro and in vivo using leaves extract and isolated antioxidants.
    METHODS AND RESULTS:
    A water extract of the leaves of T. catappa showed a strong radical scavenging action for 1,1-diphenyl-2-picrylhydrazyl and superoxide (O(2)(.-)) anion. Chebulagic acid and Corilagin were isolated as the active components from T. catappa. Both antioxidants showed a strong scavenging action for O(2)(.-) and peroxyl radicals and also inhibited reactive oxygen species production from leukocytes stimulated by phorbol-12-myristate acetate. Galactosamine (GalN, 600 mg/kg, s.c.,) and lipopolysaccharide (LPS, 0.5 microg/kg, i.p.)-induced hepatotoxicity of rats as seen by an elevation of serum alanine aminotransferase, aspartate aminotransferase and glutathione S-transferase (GST) activities was significantly reduced when the herb extract or Corilagin was given intraperitoneally to rats prior to GalN/LPS treatment. Increase of free radical formation and lipid peroxidation in mitochondria caused by GalN/LPS treatment were also decreased by pretreatment with the herb/Corilagin. In addition, apoptotic events such as DNA fragmentation and the increase in caspase-3 activity in the liver observed with GalN/LPS treatment were prevented by the pretreatment with the herb/Corilagin.
    CONCLUSIONS:
    These results show that the extract of T. catappa and its antioxidant, Corilagin are protective against GalN/LPS-induced liver injury through suppression of oxidative stress and apoptosis.
    Mol Neurobiol. 2014 Nov 4.
    Corilagin Protects Against HSV1 Encephalitis Through Inhibiting the TLR2 Signaling Pathways In Vivo and In Vitro.[Pubmed: 25367881]
    In this study, we tried to explore the molecular mechanism that Corilagin protected against herpes simplex virus-1 encephalitis through inhibiting the TLR2 signaling pathways in vivo and in vitro.
    METHODS AND RESULTS:
    As a result, Corilagin significantly prevented increase in the levels of TLR2 and its downstream mediators following Malp2 or HSV-1 challenge. On the other hand, in spite of TLR2 knockdown, Corilagin could still significantly suppress the expression of P38 and NEMO, phosphor-P38, and nuclear factor kappa B. The mRNA and protein expression of TLR2 and its downstream mediators in the brain tissue were also significantly lowered in mice treated with Corilagin. In addition, Corilagin inhibited expression of tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 protein.
    CONCLUSIONS:
    In conclusion, Corilagin shows the potential to protect against HSV-1-induced encephalitis, and the beneficial effects may be mediated by inhibiting TLR2 signaling pathways.
    Cell Biol Int. 2013 Oct;37(10):1046-54.
    Corilagin inhibits hepatocellular carcinoma cell proliferation by inducing G2/M phase arrest.[Pubmed: 23686743]
    Hepatocellular carcinoma (HCC) is one of most common types of malignant tumours. Therefore, it is very important to identify powerful drugs and their antitumour mechanisms. Corilagin has a significant antitumour potential and lower toxicity in normal cells in vitro.
    METHODS AND RESULTS:
    The IC50 values of Corilagin for normal Chang-liver cells and the HCC cell lines Bel7402 and SMMC7721 were 131.4, 24.5 and 23.4 μM, respectively, in the methyl thiazolyl tetrazolium (MTT) assay. MHCC97-H xenografts in Balb/c mice intraperitoneally injected with 30 mg/kg Corilagin for 5 weeks showed a 47.3% inhibition of tumour growth in vivo. Furthermore, data from flow cytometry and Western blot analyses of cell cycle and cell cycle-related proteins suggest that Corilagin arrests SMMC7721 cells at the G2/M phase by downregulating p-Akt and cyclin B1/cdc2 and upregulating p-p53 and p21(Cip1) .
    CONCLUSIONS:
    In conclusion, Corilagin is a potential antitumour drug that is effective in retarding the growth of HCC, which is correlated with the activation of p-p53-p21(Cip1) -cdc2/cyclin B1.
    Yakugaku Zasshi. 2005 Jul;125(7):587-91.
    Antiatherogenic effects of phyllanthus emblica associated with corilagin and its analogue.[Pubmed: 15997216]
    Oxidized low-density lipoprotein (ox-LDL) is the main etiologic factor in atherogenesis, and antioxidants are accepted as effective treatment of atherosclerosis. The aim of this study was to clarify whether the mechanism of the antiatherogenic effects of the herb Phyllanthus Emblica, which is widely used to treat atherosclerosis-related diseases, is associated with ox-LDL via its compounds of soluble tannin, Corilagin (beta-1-O-galloyl-3,6-(R)-hexahydroxydiphenoyl-d-glucose), and its analogue Dgg16 (1,6-di-O-galloyl-beta-d-glucose).
    METHODS AND RESULTS:
    Human umbilical vein endothelial cells, ECV-304, were incubated with ox-LDL (50 mg/l), treated with Corilagin or Dgg16 at different doses (0.0001-0.1 mmol/l), and then incubated with monocytes. Malondialdehyde (MDA) in the culture media was determined and the number of monocytes adhering to ECV-304 cells was counted with cytometry. In another experiment, the rat vascular smooth muscular cells (VSMC) were incubated in media with or without ox-LDL (50 mg/l), and with Corilagin or Dgg16 also at different doses (0.0001-0.1 mol/l), the proliferation of which was assayed with MTT. The results showed that both Corilagin and Dgg16 were able to decrease MDA, prevented ECV-304 cells from being adhering to by monocytes, and inhibited VSMC proliferation activated by ox-LDL.
    CONCLUSIONS:
    The results suggest that the two compounds are effective in inhibiting the progress of atherosclerosis by alleviating oxidation injury or by inhibiting ox-LDL-induced VSMC proliferation, which may be promising mechanisms for treating atherosclerosis.
    Can J Physiol Pharmacol. 1995 Oct;73(10):1425-9.
    Antihypertensive effect of corilagin in the rat.[Pubmed: 8748933]
    The antihypertensive effect of Corilagin, one of the ellagitannins purified from the seeds of Euphoria longana Lam. (Sapindaceae), was investigated in the spontaneously hypertensive rat (SHR).
    METHODS AND RESULTS:
    Administration of Corilagin into conscious SHR at 5 mg/kg produced an antihypertensive effect equivalent to that induced by 1 mg/kg of guanethidine. This dose-dependent hypotensive effect was comparable with that observed in anesthetized SHR animals. Corilagin did not modify the baroreflex sensitivity in phenylephrine-challenged SHR. Corilagin reduced plasma noradrenaline in a dose-dependent fashion, an effect that was maintained in adrenalectomized rats. Failure of the antagonists for alpha2-adrenoceptors, idazoxan and yohimbine, as well as for dopamine receptors, haloperidol and domperidone, to reverse the antihypertensive actions of Corilagin ruled out the participation of these receptors. Moreover, Corilagin attenuated the pressor effects of methoxamine and Bay K8644 to a similar degree, indicating the direct effect of Corilagin on vascular activity in rats.
    CONCLUSIONS:
    These results suggest that Corilagin possesses the ability to lower blood pressure through the reduction of noradrenaline release and (or) direct vasorelaxation.
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