Armepavine
(Synonyms: 亚美罂粟碱；杏黄罂粟碱；亚美尼亚罂粟碱；亚美异粟碱) 目录号 : GC35394
Armepavine 是一种来自 Nelumbo nucifera 的活性化合物，不仅对人外周血单核细胞具有抗炎作用，且对 T 淋巴细胞和狼疮肾炎小鼠也具有免疫抑制作用。Armepavine 抑制 TNF-α 诱导的 MAPK 和 NF-κB 信号级联反应。
Cas No.:524-20-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Armepavine, an active compound from Nelumbo nucifera, exerts not only anti-inflammatory effects on human peripheral blood mononuclear cells, but also immunosuppressive effects on T lymphocytes and on lupus nephritic mice. Armepavine inhibits TNF-α-induced MAPK and NF-κB signaling cascades[1]. p65
[1]. Weng TC, et al. Inhibitory effects of armepavine against hepatic fibrosis in rats. J Biomed Sci. 2009 Sep 2;16:78.
| Cas No. | 524-20-9 | SDF | |
| 别名 | 亚美罂粟碱；杏黄罂粟碱；亚美尼亚罂粟碱；亚美异粟碱 | ||
| Canonical SMILES | OC(C=C1)=CC=C1C[C@@H]2C3=CC(OC)=C(OC)C=C3CCN2C | ||
| 分子式 | C19H23NO3 | 分子量 | 313.39 |
| 溶解度 | Soluble in DMSO | 储存条件 | 4°C, protect from light |
| 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 | 3.1909 mL | 15.9546 mL | 31.9091 mL |
| 5 mM | 0.6382 mL | 3.1909 mL | 6.3818 mL |
| 10 mM | 0.3191 mL | 1.5955 mL | 3.1909 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。
Determination of Armepavine in mouse blood by UPLC-MS/MS and its application to pharmacokinetic study
Biomed Chromatogr 2018 May 3;e4273.PMID:29726027DOI:10.1002/bmc.4273.
The purpose of this study was to develop an ultra-performance liquid chromatography with tandem mass spectrometry (UPLC-MS/MS) method to determine Armepavine in mouse blood. Nuciferine was used as internal standard. Chromatographic separation was performed on a UPLC BEH (2.1 × 50 mm, 1.7 μm) column with a gradient elution of acetonitrile and 10 mmol/L ammonium acetate solution (containing 0.1% formic acid). The quantitative analysis was conducted in multiple reaction monitoring mode with m/z 314.1 → 106.9 for Armepavine and m/z 296.2 → 265.1 for nuciferine. Calibration curves were linear (r > 0.995) over the concentration range 1-1000 ng/mL in mouse blood with a lowest limit of quantitation of 1 ng/mL. The intra- and inter-day precisions of Armepavine in mouse were < 13.5 and 10.8%, respectively. The accuracy ranged between 86.8 and 103.3%. Meanwhile, the average recovery was >70.7% and the matrix effect was within the range 109.5-113.7%. All of the obtained data confirmed the satisfactory sensitivity and selectivity of the developed method which was then successfully applied to evaluate the pharmacokinetic behavior of Armepavine in mouse for the first time. The bioavailability of Armepavine in mouse was calculated to be 11.3%.
Armepavine oxalate induces cell death on CCRF-CEM leukemia cell line through an apoptotic pathway
Life Sci 2004 Jun 18;75(5):549-57.PMID:15158365DOI:10.1016/j.lfs.2003.12.017.
Drug-induced cell death can occur as a result of DNA damage, which in turn may lead to the reduction of bcl-2 expression and activation of caspase-3 expression. In the present study, we investigated the effect of armepavines and atherosperminine on the cell survival rate and expression of bcl-2 and caspase-3 in CCRF-CEM cells. Our data have revealed that Armepavine oxalate reduced the survival rate of CCRF-CEM cells in a dose- and time-dependent manner by MTT assay. However, no significant effects of Armepavine MeI and atherosperminine N-oxide on the survival rate of the CCRF-CEM cell were observed. Armepavine oxalate-induced cell death was considered to be apoptotic on the basis of observed formation of the DNA ladder and the typical apoptotic morphological change by Hoechst 33258 staining. The expression of bcl-2 protein in CCRF-CEM cells treated with 30 microM Armepavine oxalate was significantly decreased in western blotting analysis. In contrast, the expression of active caspase-3 in the cells was increased by Armepavine oxalate in a dose-dependent manner. These findings indicate the involvement of bcl-2 and caspase-3 in the apoptotic process of CCRF-CEM cells induced by Armepavine oxalate. The increased expression of active caspase-3 as well as decreased expression of bcl-2 support the assumption the Armepavine oxalate-treated cells may be capable to complete the entire apoptotic process ending in cell fragmentation.
Inhibitory effects of Armepavine against hepatic fibrosis in rats
J Biomed Sci 2009 Sep 2;16(1):78.PMID:19723340DOI:10.1186/1423-0127-16-78.
Activation of hepatic stellate cells (HSCs) plays a crucial role in liver fibrogenesis. Armepavine (Arm, C19H23O3N), an active compound from Nelumbo nucifera, has been shown to exert immunosuppressive effects on T lymphocytes and on lupus nephritic mice. The aim of this study was to investigate whether Arm could exert anti-hepatic fibrogenic effects in vitro and in vivo. A cell line of rat HSCs (HSC-T6) was stimulated with tumor necrosis factor-alpha (TNF-alpha) or lipopolysaccharide (LPS) to evaluate the inhibitory effects of Arm. An in vivo therapeutic study was conducted in bile duct-ligated (BDL) rats. BDL rats were given Arm (3 or 10 mg/kg) by gavage twice daily for 3 weeks starting from the onset of BDL. Liver sections were taken for fibrosis scoring, immuno-fluorescence staining and quantitative real-time mRNA measurements. In vitro, Arm (1-10 microM) concentration-dependently attenuated TNF-alpha- and LPS-stimulated alpha-SMA protein expression and AP-1 activation by HSC-T6 cells without adverse cytotoxicity. Arm also suppressed TNF-alpha-induced collagen collagen deposition, NFkappaB activation and MAPK (p38, ERK1/2, and JNK) phosphorylations. In vivo, Arm treatment significantly reduced plasma AST and ALT levels, hepatic alpha-SMA expression and collagen contents, and fibrosis scores of BDL rats as compared with vehicle treatment. Moreover, Arm attenuated the mRNA expression levels of col 1alpha2, TGF-beta1, TIMP-1, ICAM-1, iNOS, and IL-6 genes, but up-regulated metallothionein genes. Our study results showed that Arm exerted both in vitro and in vivo antifibrotic effects in rats, possibly through anti-NF-kappaB activation pathways.
Effects of Armepavine against hepatic fibrosis induced by thioacetamide in rats
Phytother Res 2012 Mar;26(3):344-53.PMID:21717514DOI:10.1002/ptr.3539.
The aim of this study was to investigate if Armepavine (Arm, C₁₉H₂₃O₃N) could exert inhibitory effects against hepatic fibrosis in rats. A cell line of rat hepatic stellate cells (HSC-T6) was stimulated with tumour necrosis factor-α (TNF-α) to evaluate the inhibitory effects of Arm. Rats were injected with thioacetamide (TAA; 300 mg/kg, intraperitoneally) thrice a week for 4 weeks to induce hepatic fibrosis, with Arm (3 or 10 mg/kg) given by gavage twice a day. Liver sections were taken for western blotting, fibrosis scoring and immunofluorescence staining. Arm (1-10 µm) concentration-dependently attenuated TNF-α-stimulated: (i) protein expressions of α-smooth muscle actin (α-SMA), collagen type I and angiopoietin-1; (ii) H₂O₂ production; and (iii) NF-κB, JunD and C/EBPß (cytidine-cytidine-adenosine-adenosine-thymidine (CCAAT)/enhancer binding protein-ß (EBPß)) nuclear translocations in HSC-T6 cells. In vivo Arm treatment significantly reduced plasma aspartate transaminase and alanine transaminase levels, hepatic α-SMA expression and collagen contents, and fibrosis scores of TAA-injected rats. Moreover, Arm treatment decreased α-SMA- and NF-κB-positive cells in immunohistochemical staining, and mRNA expression levels of IL-6, TGF-ß1, TIMP-1, col1α2, iNOS and ICAM-1 genes, but up-regulated the metallothionein gene in the livers of TAA-injected rats. Our results indicated that Arm exerted both in vitro and in vivo antifibrotic effects in rats, with inhibition of NF-κB, JunD and C/EBPß pathways.
Bisbenzylisoquinoline alkaloids and P-glycoprotein function: A structure activity relationship study
Bioorg Med Chem 2020 Jun 15;28(12):115553.PMID:32503690DOI:10.1016/j.bmc.2020.115553.
Conflicts with the notion that specific substrate interactions were required in the control of reaction path in active transport systems, P-glycoprotein showed extraordinarily low specificity. Therefore, overexpression P-glycoprotein excluded a large number of anticancer agents from cancer cells, and multidrug resistance happened. Several kinds of bisbenzylisoqunoline alkaloids were reported to modulate P-glycoprotein function and reverse drug resistance. In order to provide more information for their structure activity relationship on P-glycoprotein function, the effects of tetrandrine, isotetrandrine, fangchinoline, berbamine, dauricine, cepharanthine and Armepavine on the P-glycoprotein function were compared by using daunorubicin-resistant leukemia MOLT-4 cells in the present study. Among them, tetrandrine exhibited the strongest P-glycoprotein inhibitory effect, followed with fangchinoline and cepharanthine, and subsequently with berbamine or isotetrandrine. However, dauricine and Armepavine showed little influence on the P-glycoprotein function. These data revealed that the 18-membered ring of the bisbenzylisoquinoline alkaloids maintained the P-glycoprotein inhibitory activity, suggesting that double isoquinoline units connected by two oxygen bridges were indispensable. Moreover, stereo-configuration of bisbenzylisoquinoline 3D structures determined their inhibitory activities, which provided a new viewpoint to recognize the specificity of binding pocket in P-glycoprotein. Our data also indicated that 3D chemical structure was more sensitive than 2D to predict the P-glycoprotein inhibitory-potencies of bisbenzylisoqunoline alkaloids.