|Source:||The herbs of Eclipta prostrata.|
|Biological Activity or Inhibitors:||1. Wedelolactone has anti-inflammatory, growth inhibitory, and pro-apoptotic effects.
2. Wedelolactone inhibits adipogenic differentiation through ERK pathway, may be a novel inhibitory effect on adipogenic differentiation in hAMSCs.
3. Wedelolactone acts as phytoestrogen in breast cancer cells by stimulating ER genomic and non-genomic signalling pathways.
4. Wedelolactone is an anti-cancer agent for breast and prostate carcinomas in vitro and in vivo targeting multiple cellular proteins including androgen receptors, 5-lipoxygenase and topoisomerase IIα.
5. Wedelolactone exhibits anti-fibrotic effects, it can significantly inhibit the activation of LX-2 cells, the underlying mechanisms of which included inducing Bcl-2 family involved apoptosis, up-regulating phosphorylated status of ERK and JNK expressions, and inhibiting NF-κB mediated activity.
6. Wedelolactone is a potent Î2-arrestin-biased G protein-coupled receptor-35 (GPR35) agonist, GPR35 has been shown to be a target of the asthma drugs cromolyn disodium and nedocromil sodium.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||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: firstname.lastname@example.org
|After receiving:||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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||3.1817 mL||15.9084 mL||31.8167 mL||63.6335 mL||79.5418 mL|
|5 mM||0.6363 mL||3.1817 mL||6.3633 mL||12.7267 mL||15.9084 mL|
|10 mM||0.3182 mL||1.5908 mL||3.1817 mL||6.3633 mL||7.9542 mL|
|50 mM||0.0636 mL||0.3182 mL||0.6363 mL||1.2727 mL||1.5908 mL|
|100 mM||0.0318 mL||0.1591 mL||0.3182 mL||0.6363 mL||0.7954 mL|
J Ethnopharmacol. 2014 Nov 18;157:206-11.
|Inhibitory effect of Ecliptae herba extract and its component wedelolactone on pre-osteoclastic proliferation and differentiation.[Pubmed: 25267578]|
|To investigate the effect of ethyl acetate extract of Ecliptae herba (EAE) and its component Wedelolactone on proliferation and differentiation of preosteoclastic RAW264.7 cells as well as proliferation of bone marrow stromal cells (BMSC). MATERIALS AND METHODS: RAW264.7 and BMSC were examined for proliferation by a 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) method. Tartrate-resistant acid phosphatase (TRAP) activity of RAW264.7 was measured by using p-nitrophenyl sodium phosphate (pNPP) assay after the cells were treated with 30ng/ml receptor activator for nuclear factor-κ B ligand (RANKL) plus various concentrations of EAE, Wedelolactone or alendronate. The formation of multinucleated TRAP-positive RAW264.7 cells was observed by using a TRAP-staining kit. RESULTS: Treatment of RAW264.7 cells with EAE at high doses (20µg/ml and 40µg/ml) or Wedelolactone at 10µg/ml resulted in a decrease in proliferation of RAW264.7 cells. Low doses of EAE (5, 10µg/ml) and Wedelolactone (2.5µg/ml) inhibited RANKL-induced TRAP activity by 20.3%, 37.9%, and 48.3%. The inhibitory effect of Wedelolactone is more potent than that of alendronate, an anti-resorptive drug. Morphological changes revealed that 5µg/ml EAE and 2.5µg/ml Wedelolactone reduced the number of multinucleated osteoclast-like cells. At the high doses, EAE (20µg/ml) and Wedelolactone (10µg/ml) inhibited the growth of BMSC. CONCLUSIONS: EAE and its component Wedelolactone inhibited osteoclast RAW264.7 proliferation and differentiation at the low doses, but at the high doses, showed cytotoxic effect on BMSC. These results indicated that EAE and wedelolatone might be potential alternative therapy for osteoporosis.|
J Steroid Biochem Mol Biol. 2015 Apr 28;152:76-83.
|Wedelolactone induces growth of breast cancer cells by stimulation of estrogen receptor signalling.[Pubmed: 25934092]|
|Wedelolactone, a plant coumestan, was shown to act as anti-cancer agent for breast and prostate carcinomas in vitro and in vivo targeting multiple cellular proteins including androgen receptors, 5-lipoxygenase and topoisomerase IIα. It is cytotoxic to breast, prostate, pituitary and myeloma cancer cell lines in vitro at μM concentrations. In this study, however, a novel biological activity of nM dose of Wedelolactone was demonstrated. Wedelolactone acts as agonist of estrogen receptors (ER) α and β as demonstrated by transactivation of estrogen response element (ERE) in cells transiently expressing either ERα or ERβ and by molecular docking of this coumestan into ligand binding pocket of both ERα and ERβ. In breast cancer cells, Wedelolactone stimulates growth of estrogen receptor-positive cells, expression of estrogen-responsive genes and activates rapid non-genomic estrogen signalling. All these effects can be inhibited by pretreatment with pure ER antagonist ICI 182,780 and they are not observed in ER-negative breast cancer cells. We conclude that Wedelolactone acts as phytoestrogen in breast cancer cells by stimulating ER genomic and non-genomic signalling pathways.|
Eur J Pharmacol. 2013 Aug 15;714(1-3):105-11.
|Wedelolactone exhibits anti-fibrotic effects on human hepatic stellate cell line LX-2.[Pubmed: 23791612]|
|Wedelolactone is a major coumarin of Eclipta prostrata, which is used for preventing liver damage. However the effects of Wedelolactone on hepatic fibrosis remained unexplored. The purpose of this study was to demonstrate the anti-fibrotic effects of Wedelolactone on activated human hepatic stellate cell (HSC) line LX-2 and the possible underlying mechanisms by means of MTT assay, Hoechst staining, as well as real-time quantitative PCR and western blot. The results showed that Wedelolactone reduced the cellular viability of LX-2 in a time and dose-dependent manner. After treatment of Wedelolactone, the expressions of collagen I and α-smooth muscle actin, two biomarkers of LX-2 activation, were remarkably decreased. The apoptosis of LX-2 cells was induced by Wedelolactone accompanied with the decreasing expression of anti-apoptotic Bcl-2 and increasing expression of pro-apoptotic Bax. In addition, phosphorylated status of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) was up-regulated, but not in p38. Moreover, Wedelolactone significantly repressed the level of phosphorylated inhibitor of nuclear factor κB (IκB) and p65 in nucleus in spite of tumor necrosis factor-α stimulation. In conclusion, Wedelolactone could significantly inhibit the activation of LX-2 cells, the underlying mechanisms of which included inducing Bcl-2 family involved apoptosis, up-regulating phosphorylated status of ERK and JNK expressions, and inhibiting nuclear factor-κB (NF-κB) mediated activity. Wedelolactone might present as a useful tool for the prevention and treatment of hepatic fibrosis.|
J Cell Biochem. 2012 Nov;113(11):3436-45.
|Wedelolactone inhibits adipogenesis through the ERK pathway in human adipose tissue-derived mesenchymal stem cells.[Pubmed: 22678810]|
|Wedelolactone is an herbal medicine that is used to treat septic shock, hepatitis and venom poisoning. Although in differentiated and cancer cells, Wedelolactone has been identified as anti-inflammatory, growth inhibitory, and pro-apoptotic, the effects of Wedelolactone on stem cell differentiation remain largely unknown. Here, we report that Wedelolactone inhibits the adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells (hAMSCs). Wedelolactone reduced the formation of lipid droplets and the expression of adipogenesis-related proteins, such as CCAAT enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), lipoprotein lipase (LPL), and adipocyte fatty acid-binding protein aP2 (aP2). Wedelolactone mediated this process by sustaining ERK activity. In addition, inhibition of ERK activity with PD98059 resulted in reversion of the Wedelolactone-mediated inhibition of adipogenic differentiation. Taken together, these results indicate that Wedelolactone inhibits adipogenic differentiation through ERK pathway and suggest a novel inhibitory effect of Wedelolactone on adipogenic differentiation in hAMSCs.|
Oncotarget. 2015 May 30;6(15):13049-59.
|Wedelolactone disrupts the interaction of EZH2-EED complex and inhibits PRC2-dependent cancer.[Pubmed: 25944687]|
|Wedelolactone, binds to EED with a high affinity (KD = 2.82 μM), blocks the EZH2-EED interaction in vitro, induces the degradation of PRC2 core components and modulates the expression of detected PRC2 downstream targets and cancer-related genes. Furthermore, some PRC2-dependent cancer cells undergone growth arrest upon treatment with Wedelolactone. Thus, Wedelolactone and its derivatives which target the EZH2-EED interaction could be candidates for the treatment of PRC2-dependent cancer.|
|Anti-inflammatory gallic Acid and wedelolactone are G protein-coupled receptor-35 agonists.[Pubmed: 22488351 ]|
|G protein-coupled receptor-35 (GPR35) has been shown to be a target of the asthma drugs cromolyn disodium and nedocromil sodium. Gallic acid and caffeic acids are reported to modulate allergic reactions via unknown mode(s) of action. Here we attempt to elucidate whether both phenolic acids share a common mode of action with the two asthma drugs. Label-free dynamic mass redistribution (DMR) assays showed that both phenolic acids triggered robust DMR signals in HT-29 cells, whose characteristics were similar to that of cromolyn disodium. Both phenolic acids resulted in detectable β-arrestin translocation signals in an engineered U2OS cell line stably expressing a C-terminal-modified GPR35, but with lower efficacy than cromolyn disodium. Antiallergic Wedelolactone was found to be a potent β-arrestin-biased GPR35 agonist. These results suggest that certain anti-inflammatory phytochemicals including gallic acid and Wedelolactone may modulate inflammatory allergic action via their agonism at GPR35. GPR35 may represent a target for the treatment of allergic disorders including asthma.|