Alpinetin
(Synonyms: 山姜素) 目录号 : GC35308
Alpinetin, a composition of Alpinia katsumadai Hayata, has been reported to have a number of biological properties, such as antibacterial, antitumor and other important therapeutic activities. Alpinetin is a flavonoid isolated from Alpinia katsumadai Hayata, activates activates PPAR-γ, with potent anti-inflammatory activity.
Cas No.:36052-37-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Alpinetin, a composition of Alpinia katsumadai Hayata, has been reported to have a number of biological properties, such as antibacterial, antitumor and other important therapeutic activities. Alpinetin is a flavonoid isolated from Alpinia katsumadai Hayata, activates activates PPAR-γ, with potent anti-inflammatory activity.
Alpinetin markedly inhibits the LPS- induced TNF-α, IL-6 and IL-1β production both in vitro and vivo. Furthermore, alpinetin blocks the phosphorylation of IκBα protein, p65, p38 and extracellular signal-regulated kinase (ERK) in LPS stimulated RAW 264.7 cells[1]. Alpinetin can suppress the proliferation and invasiveness of GSCs and induce apoptosis in GSCs[2].
Alpinetin attenuates lung histopathologic changes in mouse models[1].
[1] Huo M, et al. Int Immunopharmacol. 2012, 12(1):241-8. [2] Wang J, et al. Tumour Biol. 2016, 37(7):9243-8.
| Cas No. | 36052-37-6 | SDF | |
| 别名 | 山姜素 | ||
| Canonical SMILES | O=C1C[C@@H](C2=CC=CC=C2)OC3=CC(O)=CC(OC)=C13 | ||
| 分子式 | C16H14O4 | 分子量 | 270.28 |
| 溶解度 | DMSO: 50 mg/mL (184.99 mM) | 储存条件 | Store at -20°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 | 3.6999 mL | 18.4993 mL | 36.9987 mL |
| 5 mM | 0.74 mL | 3.6999 mL | 7.3997 mL |
| 10 mM | 0.37 mL | 1.8499 mL | 3.6999 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。
Alpinetin: A Review of Its Pharmacology and Pharmacokinetics
Front Pharmacol 2022 Feb 4;13:814370.PMID:35185569DOI:10.3389/fphar.2022.814370.
Flavonoids isolated from medicinal herbs have been utilized as valuable health-care agents due to their virous biological applications. Alpinetin is a natural flavonoid that emerges in many widely used medicinal plants, and has been frequently applied in Chinese patent drugs. Accumulated evidence has demonstrated that Alpinetin possesses a broad range of pharmacological activities such as antitumor, antiinflammation, hepatoprotective, cardiovascular protective, lung protective, antibacterial, antiviral, neuroprotective, and other properties through regulating multiple signaling pathways with low systemic toxicity. However, pharmacokinetic studies have documented that Alpinetin may have poor oral bioavailability correlated to its extensive glucuronidation. Currently, the reported pharmacological properties and pharmacokinetics profiles of Alpinetin are rare to be scientifically reviewed. In this article, we aimed to highlight the mechanisms of action of Alpinetin in various diseases to strongly support its curative potentials for prospective clinical applications. We also summarized the pharmacokinetics properties and proposed some viable strategies to convey an appreciable reference for future advances of Alpinetin in drug development.
Alpinetin improves intestinal barrier homeostasis via regulating AhR/suv39h1/TSC2/mTORC1/autophagy pathway
Toxicol Appl Pharmacol 2019 Dec 1;384:114772.PMID:31676321DOI:10.1016/j.taap.2019.114772.
The injury of intestinal epithelial barrier is considered as the key pathophysiological process in response to gastrointestinal infection and inflammation, and plays an important role in the initiation and development of colitis. Alpinetin has been shown to improve intestinal barrier homeostasis under colitis condition, but the mechanism is still unclear. Here, we showed that Alpinetin significantly improved transepithelial electrical resistance (TEER) in TNF-α-stimulated Caco-2 cells, which was mainly mediated by inhibiting the apoptosis. Mechanistic studies demonstrated that Alpinetin markedly increased the production of autophagosomes, along with obvious regulation of LC3B-II, beclin-1, p62, Atg7 and Atg5 expressions. In addition, it also markedly repressed the activation of mTORC1 signaling pathway, which was ascribed to TSC2 rather than p-AKT, p-ERK, p-AMPKα or PTEN expressions in Caco-2 and NCM460 cells. Furthermore, the enrichment of H3K9me3 at TSC2 promoter region was decreased and ubiquitin proteasome degradation of suv39h1 was increased. Additionally, Alpinetin activated aryl hydrocarbon receptor (AhR) and promoted co-localization of AhR with suv39h1 in the cytoplasm. The relationship between alpinetin-regulated AhR/suv39h1/TSC2/mTORC1 signals, autophagy and apoptosis of Caco-2 and NCM460 cells was confirmed by using CH223191, siAhR, siTSC2 and chloroquine. Finally, CH223191 and leucine abolished alpinetin-mediated inhibition of intestinal epithelial cells apoptosis, improvement of intestinal epithelial barrier and amelioration of colitis.
Alpinetin exerts anti-colitis efficacy by activating AhR, regulating miR-302/DNMT-1/CREB signals, and therefore promoting Treg differentiation
Cell Death Dis 2018 Aug 30;9(9):890.PMID:30166541DOI:10.1038/s41419-018-0814-4.
Alpinetin, a flavonoid compound extracted from the seeds of Alpinia katsumadai Hayata, has been demonstrated to exert massive biological properties. This study aimed to evaluate the effect of Alpinetin on dextran sulfate sodium (DSS)-induced colitis, and elucidate the potential mechanisms. Alpinetin significantly alleviated colitis in mice, accompanied with restored Th17/Treg balance in colons. In vitro, Alpinetin directly promoted Treg differentiation but exerted little effect on Th17 differentiation, and the action was in an aryl hydrocarbon receptor (AhR)-dependent manner. It acted as a potential AhR activator, evidenced by increased expression of CYP1A1, dissociation of AhR/HSP90 complexes, AhR nuclear translocation, XRE-driven luciferase reporter gene and DNA-binding activity of AhR/ARNT/XRE in T cells. Furthermore, Alpinetin significantly promoted expression of miR-302 but not others, and restrained expression of DNMT-1 and methylation level of Foxp3 promoter region in CD4+ T cells and colons of colitis mice. However, the association of CREB and Foxp3 promoter region but not expression, nuclear translocation and DNA-binding activity of CREB was up-regulated by Alpinetin in CD4+ T cells. The relationship of alpinetin-adjusted AhR activation, expressions of miR-302 and DNMT-1, association of CREB and Foxp3 promoter region, and Treg differentiation was confirmed by using CH223191, siAhR, miR-302 inhibitor and pcDNA3.1(+)-mDNMT-1. Finally, CH223191 abolished the amelioration of Alpinetin on colitis, induction of Treg cells and regulation of miR-302/DNMT-1/CREB signals in colons of colitis mice. In conclusion, Alpinetin ameliorated colitis in mice via activating AhR, regulating miR-302/DNMT-1/CREB signals, therefore promoting Treg differentiation.
Alpinetin: a Dietary Flavonoid with Diverse Anticancer Effects
Appl Biochem Biotechnol 2022 Sep;194(9):4220-4243.PMID:35567708DOI:10.1007/s12010-022-03960-2.
Cancer is a global burden and mechanistically complex disease with a plethora of genetic, physiological, metabolic, and environmental alterations. The development of dietary nutraceuticals into cancer chemotherapeutics has emerged as a new paradigm in cancer treatment. Alpinetin (ALPI) is a novel flavonoid component of multiple edible and medicinal plants and possesses a wide range of biological and pharmacological activities including antibacterial, anti-hemostatic, anti-oxidative, anti-hepatotoxic, stomachic, immunosuppressive, and anti-inflammatory. Recently, ALPI has been reported as a bioactive dietary nutraceutical with promising anticancer activity in various human cancers through multiple mechanisms. The purpose of this review is to compile the data on natural sources of ALPI, and its anticancer activity including cellular targets and anticancer mechanism in various human cancers. Moreover, this review will set the stage for further design and conduct pre-clinical and clinical trials to develop ALPI into a lead structure for oncological therapy.
Alpinetin ameliorates bone loss in LPS-induced inflammation osteolysis via ROS mediated P38/PI3K signaling pathway
Pharmacol Res 2022 Oct;184:106400.PMID:35988868DOI:10.1016/j.phrs.2022.106400.
Background and objective: Bone loss occurs in several inflammatory diseases because of chronic persistent inflammation that activates osteoclasts (OCs) to increase bone resorption. Currently available antiresorptive drugs have severe side effects or contraindications. Herein, we explored the effects and mechanism of Alpinetin (Alp) on receptor activator of nuclear factor κB ligand (RANKL)-mediated OCs differentiation, function, and in inflammatory osteolysis of mice. Method: Primary mouse bone marrow-derived macrophages (BMMs) induced by RANKL and macrophage colony-stimulating factor (M-CSF) were utilized to test the impact of Alp on OCs differentiation, function, and intracellular reactive oxygen species (ROS) production, respectively. Expression of oxidant stress relevant factors and OCs specific genes were assessed via real-time quantitative PCR. Further, oxidative stress-related factors, NF-κB, MAPK, PI3K/AKT/GSK3-β, and NFATc1 pathways were examined via Western blot. Finally, LPS-induced mouse calvarial osteolysis was used to investigate the effect of Alp on inflammatory osteolysis in vivo. Result: Alp suppressed OCs differentiation and resorption function, and down-regulated the ROS production. Alp inhibited IL-1β, TNF-α and osteoclast-specific gene transcription. It also blocked the gene and protein expression of Nox1 and Keap1, but enhanced Nrf2, CAT, and HO-1 protein levels. Additionally, Alp suppressed the phosphorylation of PI3K and P38, and restrained the expression of osteoclast-specific gene Nfatc1 and its auto-amplification, hence minimizing LPS-induced osteolysis in mice. Conclusion: Alp is a novel candidate or therapeutics for the osteoclast-associated inflammatory osteolytic ailment.