Lucidone

Lucidone
Product Name Lucidone
CAS No.: 19956-53-7
Catalog No.: CFN98011
Molecular Formula: C15H12O4
Molecular Weight: 256.3 g/mol
Purity: >=98%
Type of Compound: Chalcones
Physical Desc.: Yellow powder
Targets: ROS | DNA/RNA Synthesis | Nrf2 | PGE | COX | NF-kB | IkB | ERK | p38MAPK | HCV | PPAR | AP-1 | GLUT | NO | TNF-α | HO-1 | TNF-α | NOS | JNK | Wnt/β-catenin | GSK-3 | CDK | p21 | MMP(e.g.TIMP) | PI3K | VEGFR | Akt | IKK
Source: The roots of Lindera strychnifolia
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price:
Lucidone possesses hepatoprotective, antioxidant and anti-inflammatory properties, it-mediated up-regulation of phase-II enzymes and HO-1 via Nrf-2 signaling pathway may provide a pivotal mechanism for its hepatoprotective action. Dietary intake of lucidone alleviates high fat diet-induced obesity in C57BL/6 mice and reveals the potential of lucidone as a nutraceutical to prevent obesity and consequent metabolic disorders. Lucidone accelerates wound healing through the cooperation of keratinocyte/fibroblast/ ndothelial cell growth and migration and macrophage inflammation via PI3K/AKT, Wnt/β-catenin and NF-κB signaling cascade activation. Lucidone also suppresses hepatitis C virus replication by Nrf2-mediated heme oxygenase-1 induction, it could be a potential lead or supplement for the development of new anti-HCV agent in the future.
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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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  • Lucidone

    Catalog No: CFN98011
    CAS No: 19956-53-7
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    Antimicrob Agents Chemother. 2013 Mar;57(3):1180-91.
    Lucidone suppresses hepatitis C virus replication by Nrf2-mediated heme oxygenase-1 induction.[Pubmed: 23254429]

    METHODS AND RESULTS:
    Upon screening of plant-derived natural products against hepatitis C virus (HCV) in the replicon system, we demonstrate that Lucidone, a phytocompound, isolated from the fruits of Lindera erythrocarpa Makino, significantly suppressed HCV RNA levels with 50% effective concentrations of 15 ± 0.5 μM and 20 ± 1.1 μM in HCV replicon and JFH-1 infectious assays, respectively. There was no significant cytotoxicity observed at high concentrations, with a 50% cytotoxic concentration of 620 ± 5 μM. In addition, Lucidone significantly induced heme oxygenase-1 (HO-1) production and led to the increase of its product biliverdin for inducing antiviral interferon response and inhibiting HCV NS3/4A protease activity. Conversely, the anti-HCV activity of Lucidone was abrogated by blocking HO-1 activity or silencing gene expression of HO-1 or NF-E2-related factor 2 (Nrf2) in the presence of Lucidone, indicating that the anti-HCV action of Lucidone was due to the stimulation of Nrf-2-mediated HO-1 expression. Moreover, the combination of Lucidone and alpha interferon, the protease inhibitor telaprevir, the NS5A inhibitor BMS-790052, or the NS5B polymerase inhibitor PSI-7977, synergistically suppressed HCV RNA replication.
    CONCLUSIONS:
    These findings suggest that Lucidone could be a potential lead or supplement for the development of new anti-HCV agent in the future.
    Toxicol In Vitro. 2012 Aug;26(5):700-8.
    Hepatoprotective effect of lucidone against alcohol-induced oxidative stress in human hepatic HepG2 cells through the up-regulation of HO-1/Nrf-2 antioxidant genes.[Pubmed: 22484158 ]
    Lucidone was previously reported to exhibit anti-inflammatory activity in vitro and in vivo.
    METHODS AND RESULTS:
    In the present study, we characterized the mechanisms underlying the hepatoprotective effect of Lucidone against alcohol-induced oxidative stress in vitro. Human hepatoma (HepG2) cells were pretreated with Lucidone (1-10μg/mL) and then hepatotoxicity was stimulated by the addition ethanol (100mM). With response to ethanol-challenge, increased amount of alanine aminotransferase (ALT) and aspirate aminotransferase (AST) release were observed, whereas Lucidone pretreatment significantly inhibited the leakage of AST and ALT in HepG2 cells without appreciable cytotoxic effects. We also found that Lucidone pretreatment significantly decreased ethanol-induced nitric oxide (NO), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), reactive oxygen species (ROS) and glutathione (GSH) depletion in HepG2 cells. Furthermore, Western blot and quantitative-PCR analyses showed that ethanol-exposure apparently down-regulated endogenous anti-oxidant hemoxygenase-1 (HO-1) expression, whereas pretreatment with Lucidone significantly up-regulates HO-1 expression followed by the transcriptional activation of NF-E2 related factor-2 (Nrf-2). Interestingly, the profound up-regulation of HO-1 and Nrf-2 were observed in only ethanol-challenged cells, which evidenced that Lucidone-induced induction of HO-/Nrf-2 were specific with oxidative stress.
    CONCLUSIONS:
    Thus, we concluded that Lucidone-mediated up-regulation of phase-II enzymes and HO-1 via Nrf-2 signaling pathway may provide a pivotal mechanism for its hepatoprotective action.
    Int Immunopharmacol. 2010 Apr;10(4):385-92.
    Anti-inflammatory effect of lucidone in mice via inhibition of NF-kappaB/MAP kinase pathway.[Pubmed: 20079881]

    METHODS AND RESULTS:
    Here, we investigated the anti-inflammatory activity of Lucidone, a phytocompound isolated from the fruits of Lindera erythrocarpa Makino, against lipopolysaccharide (LPS)-induced acute systemic inflammation in mice. Male ICR mice were injected intraperitoneally with LPS (5 microg/kg), and the effects of pretreatment with various concentrations of Lucidone (50-200 mg/kg) for 12h on the formation of nitric oxide (NO), prostaglandin-E(2) (PGE(2)) and tumor necrosis factor (TNF-alpha) were analyzed. Lucidone inhibited the production of NO, PGE(2) and TNF-alpha production in LPS-induced mice, and also induced mRNA and protein levels of inducible nitric oxide synthase (iNOS), and cyclooxigenase-2 (COX-2). The two common response elements of the iNOS and COX-2 genes are nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1). NF-kappaB nuclear translocation and DNA binding were inhibited by Lucidone in the LPS-induced mice. Moreover, Lucidone decreased the expression and phosphorylation of c-Jun N-terminal kinase (JNK) protein thereby causing the subsequent inhibition of AP-1 activity. Finally, our results indicated that Lucidone was able to block mitogen-activated protein kinases activity and its downstream signaling activation of NF-kappaB and AP-1.
    CONCLUSIONS:
    We thus conclude that Lucidone exerts its anti-inflammatory effects in mice by inhibiting the expression of pro-inflammatory factors and their related signaling pathways.
    Food Chem Toxicol. 2013 Sep;59:55-66.
    Lucidone protects human skin keratinocytes against free radical-induced oxidative damage and inflammation through the up-regulation of HO-1/Nrf2 antioxidant genes and down-regulation of NF-κB signaling pathway.[Pubmed: 23712098]
    We investigated the protective effects of Lucidone, a naturally occurring cyclopentenedione isolated from the fruits of Lindera erythrocarpa Makino, against free-radical and inflammation stimulator 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH)-induced oxidative stress in human keratinocyte (HaCaT) cells, with the aim of revealing the possible mechanisms underlying the protective efficacy.
    METHODS AND RESULTS:
    Lucidone pretreatment (0.5-10 μg/mL) markedly increased HaCaT cell viability and suppressed AAPH-induced reactive oxygen species (ROS) generation, lipid peroxidation, and DNA damage. Notably, the antioxidant potential of Lucidone was directly correlated with the increased expression of an antioxidant gene, heme oxygenase 1 (HO-1), which was followed by the augmentation of the nuclear translocation and transcriptional activation of NF-E2-related factor-2 (Nrf2), with or without AAPH. Nrf2 knockdown diminished the protective effects of Lucidone. We also observed that Lucidone pretreatment inhibited AAPH-induced inflammatory chemokine prostaglandin E₂ (PGE₂) production and the expression of cyclooxygenase-2 (COX-2) in HaCaT cells. Lucidone treatment also significantly inhibited AAPH-induced nuclear factor-κB (NF-κB) activation and suppressing the degradation of inhibitor-κB (I-κB). Furthermore, Lucidone significantly diminished AAPH-induced COX-2 expression through the down-regulation of the extracellular signal-regulated kinase (ERK) and p38 MAPK signaling pathways.
    CONCLUSIONS:
    Therefore, Lucidone may possess antioxidant and anti-inflammatory properties and may be useful for the prevention of free radical-induced skin damage.
    Biochim Biophys Acta. 2017 Jan;1864(1):151-168.
    Lucidone Promotes the Cutaneous Wound Healing Process via Activation of the PI3K/AKT, Wnt/β-catenin and NF-κB Signaling Pathways.[Pubmed: 27816443 ]
    Lucidone, which comprises a naturally occurring cyclopentenedione, has been investigated for its in vitro and in vivo wound healing properties, and the underlying molecular signaling cascades in the wound healing mechanism have been elucidated.
    METHODS AND RESULTS:
    We demonstrated the cell-/dose-specific responses of Lucidone (0.5-8μM) on proliferation and migration/invasion of keratinocyte HaCaT and fibroblast Hs68 cells. In keratinocytes, Lucidone-induced nuclear translocation of β-catenin was accompanied by increased transcriptional target genes, including c-Myc and cyclin-D1, through GSK3β-dependent pathway. Correspondingly, Lucidone promoted the cell-cycle by increasing PCNA/CDK4 and decreasing p21/p27 expressions. Lucidone induced EMT through the downregulation of epithelial (E-cadherin/occludin) and upregulation of mesenchymal (vimentin/Twist/Snail) marker proteins. Activated MMP-9/-2 and uPA/uPAR as well as suppressed TIMP-1/-2 and PAI-1 expressions by Lucidone may promote the migration/invasion of keratinocytes. Notably, Lucidone activated NF-κB signaling via IKK-mediated-IκB degradation, and its inhibition abolished MMP-9 activation and keratinocyte migration. Inhibition of PI3K/AKT signaling impaired the Lucidone-induced proliferation/migration with corresponding suppression of β-catenin/c-Myc/cyclin-D1 and NF-κB/MMP-9 expressions. Results indicate that Lucidone-induced PI3K/AKT signaling anchored the β-catenin/NF-κB-mediated healing mechanism. β-catenin knockdown substantially diminished Lucidone-induced keratinocyte migration. Furthermore, Lucidone increased endothelial cell proliferation/migration and triggered angiogenesis (MMP-9/uPA/ICAM-1). In macrophages, Lucidone-activated NF-κB-mediated inflammation (COX-2/iNOS/NO) and VEGF, which may contribute to the growth of keratinocytes/fibroblasts and endothelial cells. Punched wounds on mice were rapidly healed with the topical application of Lucidone (5mM) compared with control ointment-treated mice.
    CONCLUSIONS:
    Taken together, Lucidone accelerates wound healing through the cooperation of keratinocyte/fibroblast/endothelial cell growth and migration and macrophage inflammation via PI3K/AKT, Wnt/β-catenin and NF-κB signaling cascade activation.
    Phytomedicine. 2013 Mar 15;20(5):394-400.
    Lucidone from Lindera erythrocarpa Makino fruits suppresses adipogenesis in 3T3-L1 cells and attenuates obesity and consequent metabolic disorders in high-fat diet C57BL/6 mice.[Pubmed: 23265843]
    Obesity is associated with an increased risk of development of numerous diseases including type 2 diabetes, hypertension, hyperlipidemia, and cardiovascular disease.
    METHODS AND RESULTS:
    In this study, we investigated the effects of Lucidone in vitro on gene expression during adipogenesis in 3T3-L1 cells and in vivo on high-fat diet induced obesity in C57BL/6 mice. Lucidone at 40 μmol/L suppressed adipogenesis in 3T3-L1 cells by reducing transcription levels of adipogenic genes, including PPARγ, C/EBPα, LXR-α, LPL, aP2, GLUT4 and adiponectin. Five-week-old male C57BL/6 mice fed a high fat diet (60% energy from fat) supplemented with Lucidone at a dosage of 1250 mg/kg of diet for 12 weeks had reduced body and liver weight, reduced epididymal and perirenal adipose tissue, decreased food efficiency (percentage of weight gain divided by food intake), and lowered plasma cholesterol, triglyceride, glucose, and insulin levels. Dissection of adipose tissue from Lucidone-treated mice showed a reduction in the average fat-cell size and percentage of large adipocytes.
    CONCLUSIONS:
    These results provide evidence that dietary intake of Lucidone alleviates high fat diet-induced obesity in C57BL/6 mice and reveals the potential of Lucidone as a nutraceutical to prevent obesity and consequent metabolic disorders.
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