Piceatannol
(Synonyms: 白皮杉醇; Astringenin; trans-Piceatannol) 目录号 : GN10503
Piceatannol(3,3 '，4,5 ' -反式三羟基二苯乙烯)是天然存在的白藜芦醇羟基化类似物。
Cas No.:10083-24-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
Mouse brain endothelial cell line bEnd.3 |
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Preparation Method |
The bEnd.3 cells were cultured in DMEM containing 10% FBS plus 100 U/mL penicillin and 100 U/mL streptomycin at 37 °C in a humidified atmosphere with 5% CO2. Cells were subcultured every 2-3 days. All the experiments with bEnd.3 cells were performed between passages 5 to 25 for maintaining excellent BBB characteristics in vitro. The bEnd.3 cell impaired model was induced by treating with LPS at two different concentrations and stimulation times (1 µg/mL for 24 h or 10 µg/mL for 1 h) to examine different target proteins modulating inflammatory and antioxidant responses. Piceatannol (10 or 50 µM) was added to the medium for 30 min and then LPS (10 µg/mL) was added in the existing medium containing piceatannol for 1 h. For another set of experiments, cells were pretreated with piceatannol for 4 h before LPS stimulation (1 µg/mL for 24 h) in the existing medium. Piceatannol was dissolved in 1% dimethyl sulfoxide (DMSO), and LPS was dissolved in phosphate-buffered saline (PBS). |
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Reaction Conditions |
10 or 50 µM for 1.5 or 28 hours |
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Applications |
The protein expression of ICAM-1 and VCAM-1 was upregulated by LPS (1 µg/mL) exposure for 24 h, whereas such upregulation was reversed by pretreatment with 50 µM piceatannol for 4 h in bEnd.3 cells |
| Animal experiment [2]: | |
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Animal models |
Four-week-old female BALB/c mice |
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Preparation Method |
After given 2 weeks for adaption, 4T1-luc cells (5×104 cells) suspended in 0.1-ml matrigel/PBS (1:1, v/v) were injected into the inguinal mammary fat pad. One day after injection, the animals were randomly divided into three experimental groups. Piceatannol (10 or 20 mg/kg) in corn oil or corn oil (vehicle) alone was administered to the mice by oral gavage every day for 30 days. |
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Dosage form |
Oral, 10 or 20 mg/kg |
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Applications |
Tumor weights were also significantly lower in the mice administered with Piceatannol than in the control group. At the time of sacrifice, the tumor weights were 0.915±0.037 g, 0.740±0.028 g and 0.668±0.047 g in the 0-mg/kg Piceatannol, 10-mg/kg Piceatannol and 20-mg/kg Piceatannol groups, respectively. |
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References: [1]: Zhou Y, Khan H, Hoi M P M, et al. Piceatannol Protects Brain Endothelial Cell Line (bEnd. 3) against Lipopolysaccharide-Induced Inflammation and Oxidative Stress[J]. Molecules, 2022, 27(4): 1206. | |
Piceatannol (3,3′,4,5′-trans-trihydroxystilbene) is a naturally occurring hydroxylated analogue of resveratrol [1]. Piceatannol inhibited mushroom tyrosinase with IC50 value of 1.53 mM [2]. piceatannol is a spleen tyrosine kinase (Syk) inhibitor, it is often used in studies involving Syk kinase-dependent cells [3,4], especially neutrophils [5,6], macrophages [7,8] and smooth muscle cells [9,10].
Piceatannol was used to specifically inhibit Syk, which is an important adaptor of FcγR cross-linking-induced downstream signaling. Application of Piceatannol aborted cyclin D1 expression induced by FcγR cross-linking in murine bone marrow-derived macrophages (BMM) [7]. Pre-incubation of piceatannol (100 nM for 1 h) increased neutrophil adhesion in the presence of E3MPO, reversing the non-adherent phenotype of the cells [5]. piceatannol inhibited Ang II-enhanced rat aortic smooth muscle cells (RASMCs) migration, and inhibited Ang II-stimulated phosphorylation of ERK1/2, p38 MAPK and Hsp27, pretreatment with piceatannol attenuated Ang II-increased sprout outgrowth from aortic rings [9].
Piceatannol (10 or 20 mg/kg/d, 3 weeks, oral) administration significantly decreases solid tumor growth in BALB/c mice injected with 4T1 mammary cancer cells [11]. Piceatannol (20 mg/kg/d, 9 days, oral) inhibits lung metastasis of MAT-Ly-Lu (MLL) cells in nude mice [12].
References:
[1]. Piotrowska H, Kucinska M, Murias M. Biological activity of piceatannol: leaving the shadow of resveratrol[J]. Mutation Research/Reviews in Mutation Research, 2012, 750(1): 60-82.
[2]. Yokozawa T, Kim Y J. Piceatannol inhibits melanogenesis by its antioxidative actions[J]. Biological and Pharmaceutical Bulletin, 2007, 30(11).
[3]. Pavanetto M, Zarpellon A, Borgo C, et al. Regulation of serotonin transport in human platelets by tyrosine kinase Syk[J]. Cellular Physiology and Biochemistry, 2011, 27(2): 139-148.
[4]. Beckmann S, Buro C, Dissous C, et al. The Syk kinase SmTK4 of Schistosoma mansoni is involved in the regulation of spermatogenesis and oogenesis[J]. PLoS Pathogens, 2010, 6(2): e1000769.
[5]. Hayes M J, Cambridge G. An IgM class anti-neutrophil cytoplasm antibody inhibits neutrophil adhesion and apoptosis via a Syk dependent signaling cascade[J]. Molecular immunology, 2004, 41(4): 457-468.
[6]. Ortiz‐Stern A, Rosales C. FcγRIIIB stimulation promotes β1 integrin activation in human neutrophils[J]. Journal of leukocyte biology, 2005, 77(5): 787-799.
[7]. Luo Y, Pollard J W, Casadevall A. Fcγ receptor cross-linking stimulates cell proliferation of macrophages via the ERK pathway[J]. Journal of Biological Chemistry, 2010, 285(6): 4232-4242.
[8]. Gevrey J C, Isaac B M, Cox D. Syk is required for monocyte/macrophage chemotaxis to CX3CL1 (Fractalkine)[J]. The Journal of Immunology, 2005, 175(6): 3737-3745.
[9]. Lau H K F, Ho J. Regulation of plasminogen activator inhibitor‿ secretion by urokinase and tissue plasminogen activator in rat epithelioid‐type smooth muscle cells[J]. British journal of haematology, 2002, 117(1): 151-158.
[10]. Lee H M, Lee C K, Lee S H, et al. p38 mitogen-activated protein kinase contributes to angiotensin II-stimulated migration of rat aortic smooth muscle cells[J]. Journal of pharmacological sciences, 2007, 105(1): 74-81.
[11]. Song H, Jung J I, Cho H J, et al. Inhibition of tumor progression by oral piceatannol in mouse 4T1 mammary cancer is associated with decreased angiogenesis and macrophage infiltration[J]. The Journal of nutritional biochemistry, 2015, 26(11): 1368-1378.
[12]. Kwon G T, Jung J I, Song H R, et al. Piceatannol inhibits migration and invasion of prostate cancer cells: possible mediation by decreased interleukin-6 signaling[J]. The Journal of nutritional biochemistry, 2012, 23(3): 228-238.
| Cas No. | 10083-24-6 | SDF | |
| 别名 | 白皮杉醇; Astringenin; trans-Piceatannol | ||
| 化学名 | 4-[(E)-2-(3,5-dihydroxyphenyl)ethenyl]benzene-1,2-diol | ||
| Canonical SMILES | C1=CC(=C(C=C1C=CC2=CC(=CC(=C2)O)O)O)O | ||
| 分子式 | C14H12O4 | 分子量 | 244.24 |
| 溶解度 | ≥ 12.2mg/mL in DMSO | 储存条件 | Store at 2-8°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.0943 mL | 20.4717 mL | 40.9433 mL |
| 5 mM | 0.8189 mL | 4.0943 mL | 8.1887 mL |
| 10 mM | 0.4094 mL | 2.0472 mL | 4.0943 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Piceatannol: A natural stilbene for the prevention and treatment of cancer
Pharmacol Res2020 Mar;153:104635.PMID: 31926274DOI: 10.1016/j.phrs.2020.104635
The World Health Organization (WHO) has documented that cancer is the second foremost reason for death worldwide. Various factors are responsible for cancer, for instance, exposure to different physical, chemical and biological carcinogens, infections, hereditary, poor dietary habits and lifestyle etc. Cancer is a preventable disease if detected at an early stage; however, most of the cases of cancer are diagnosed at an incurable advanced or metastatic stage. According to WHO about 70 % of deaths due to cancer occur in countries with low- or middle-income. The major problems associated with the conventional therapies are cancer recurrence, development of chemoresistance, affordability, late-stage diagnosis, adverse side effects and inaccessible treatment. Thus, there is an urgent need to find alternative treatment modalities, which have easy accessibility and are affordable with minimum side effects. In this article, we reviewed the natural stilbene known as "Piceatannol" for its anticancer properties. Numerous preclinical studies have reported the potential of Piceatannol to prevent or impede the growth of various cancers originating from different organs such as brain, breast, cervical, colon, liver, lung, prostate, skin, etc. The current review primarily emphasises on the insights of Piceatannol source, chemistry, and the molecular mechanisms involved in the regression of the tumor. This review supports Piceatannol as a potential anticancer and chemopreventive agent and suggests that it can be effectively employed as a capable anti-cancer drug.
Benefits of skin application of piceatannol-A minireview
Australas J Dermatol2022 Oct 20.PMID: 36264002DOI: 10.1111/ajd.13937
The skin is the largest organ of the human body and has several functions such as barrier against external agents, the maintenance of temperature and homeostatic functions. Skin ageing is a natural process that can be influenced by environmental factors, intrinsic skin factors and lifestyle. UV light plays an important role in skin ageing and can cause spots, requiring the use of depigmenting agents. Nowadays, there is a great demand for ingredients that prevent skin ageing, with natural agents occupying a promising position. Among the natural agents, polyphenols, such as resveratrol and piceatannol, found in grapes, passion fruits and other fruits, have a huge relevance. Great benefits of piceatannol have been reported, so thus, this work focuses specifically on a review of the literature regarding the application of this polyphenol in skin care products. This polyphenol can be used in a wound-healing, or as anti-ageing, antioxidant, anti-acne and skin whitening, among other effects.
Piceatannol, a metabolite of resveratrol, attenuates atopic dermatitis by targeting Janus kinase 1
Phytomedicine2022 Feb 12;99:153981.PMID: 35235887DOI: 10.1016/j.phymed.2022.153981
Background: Piceatannol is a resveratrol metabolite commonly found in red wine, grapes. Several studies have investigated the immune-modulating effects of piceatannol on processes related to allergic reactions. However, the relationship between piceatannol and atopic dermatitis (AD) has not yet been reported. This study sought to investigate the effects of piceatannol in animal and cell line models.
Methods: AD-like symptoms and skin lesions were triggered by repeated topical treatment of Dermatophagoides farinae extract (DFE) on the skin of NC/Nga mice. The molecular mechanism of piceatannol was studied in the TNFα/IFNγ-induced HaCaT cell line.
Results: Piceatannol attenuated DFE-induced AD-like symptoms, as shown by skin thickness, dermatitis score, scratching time, and skin water loss. Histopathological analysis showed that piceatannol suppressed DFE-induced immune cell infiltration into the skin. These results occurred concomitantly with the downregulation of inflammatory markers, including serum and skin TARC and MDC. Piceatannol decreased phosphorylation of JAK-STAT protein in the TNFα/IFNγ-induced HaCaT cell line. A molecular docking study showed that piceatannol strongly interacts with JAK1, suggesting a possible mode of action.
Conclusion: The study results showed that piceatannol, a metabolite of resveratrol, attenuates atopic dermatitis and provide important implication of development of piceatannol as functional ingredients or therapeutic agents.
Piceatannol Protects Brain Endothelial Cell Line (bEnd.3) against Lipopolysaccharide-Induced Inflammation and Oxidative Stress
Molecules2022 Feb 11;27(4):1206.PMID: 35208996DOI: 10.3390/molecules27041206
Dysfunction of the blood-brain barrier (BBB) is involved in the pathogenesis of many cerebral diseases. Oxidative stress and inflammation are contributing factors for BBB injury. Piceatannol, a natural ingredient found in various plants, such as grapes, white tea, and passion fruit, plays an important role in antioxidant and anti-inflammatory responses. In this study, we examined the protective effects of piceatannol on lipopolysaccharide (LPS) insult in mouse brain endothelial cell line (bEnd.3) cells and the underlying mechanisms. The results showed that piceatannol mitigated the upregulated expression of adhesion molecules (ICAM-1 and VCAM-1) and iNOS in LPS-treated bEnd.3 cells. Moreover, piceatannol prevented the generation of reactive oxygen species in bEnd.3 cells stimulated with LPS. Mechanism investigations suggested that piceatannol inhibited NF-κB and MAPK activation. Taken together, these observations suggest that piceatannol reduces inflammation and oxidative stress through inactivating the NF-κB and MAPK signaling pathways on cerebral endothelial cells in vitro.
Piceatannol alleviate ROS-mediated PC-12 cells damage and mitochondrial dysfunction through SIRT3/FOXO3a signaling pathway
J Food Biochem2022 Mar;46(3):e13820.PMID: 34132394DOI: 10.1111/jfbc.13820
Oxidative stress-associated mitochondrial dysfunction has been identified as a major mechanism in multiple neurodegenerative diseases. This study aims to investigate the cytoprotective effects of piceatannol on ROS-mediated PC-12 cells damage and related mitochondrial dysfunction. Piceatannol treatment could significantly attenuate PC-12 cells oxidative damage and ROS-mediated cells apoptosis. Moreover, pretreatment with piceatannol effectively decreased mitochondrial membrane depolarization, cleaved-caspase 3, and increased Bcl-2 and Bcl-2/Bax compared with control H2 O2 group. Meanwhile, piceatannol treatment improved mitochondrial respiration function which led to an enhancement in the maximal respiration and spare respiratory capacity. Further mechanisms analysis showed that the protein expression of SIRT3 and its downstream protein FOXO3a were significantly increased after piceatannol addition in a dose-dependent manner. Whereas the cytoprotective role of piceatannol was markedly abolished by the SIRT3 inhibitor 3-TYP, suggesting that SIRT3/FOXO3a signaling pathway played a vital role in mediating the neuronal cytoprotective effects of piceatannol. PRACTICAL APPLICATIONS: The results of our study provide a novel insight that piceatannol could be potentially used as a promising bioactive component against oxidative damage and neurocyte apoptosis. The findings may provide theoretical basis for brain health of piceatannol consumption in some extent.