14-Deoxyandrographolide
(Synonyms: 14-去氧穿心莲内酯) 目录号 : GC35057
A diterpene lactone with diverse biological properties
Cas No.:4176-97-0
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
14-Deoxyandrographolide is a diterpene lactone that has been found in A. paniculata and has diverse biological activities, including anticancer, hepatoprotective, antioxidative, and antidiabetic properties.1,2,3,4 It inhibits the growth of HL-60 cells with a GI50 value of 25.46 ?M and is cytotoxic to T47D cells (EC50 = 2.8 ?g/ml) but not HepG2 or NCI H23 cells (EC50s = 28.3 and 26.4 ?g/ml, respectively).1,2 14-Deoxyandrographolide (10 and 25 ?M) increases AMPK phosphorylation and glucose uptake in L6 myotubes and potentiates the effect of insulin to increase cell surface levels of GLUT4 in L6-GLUT4myc cells.4 It reduces blood glucose levels in rats in a model of streptozotocin-induced diabetes and in db/db diabetic mice when administered at a dose of 100 mg/kg. 14-Deoxyandrographolide reduces ethanol-induced hepatotoxicity in rats when administered at a dose of 15 mg/kg per day for the last four weeks of an eight-week ethanol exposure period.3 It also reduces protein carbonyl and thiobarbituric acid reactive substances (TBARS) levels and increases total glutathione (GSH) levels in isolated rat hepatocytes in the same model.
1.Chen, L., Zhu, H., Wang, R., et al.ent-Labdane diterpenoid lactone stereoisomers from Andrographis paniculataJ. Nat. Prod.71(5)852-855(2008) 2.Tan, M.L., Kuroyanagi, M., Sulaiman, S.F., et al.Cytotoxic Activities of Major Diterpenoid Constituents of Andrographis paniculata. in a Panel of Human Tumor Cell LinesPharmaceutical Biology43(6)501-508(2008) 3.Mandal, S., Nelson, V.K., Mukhopadhyay, S., et al.14-Deoxyandrographolide targets adenylate cyclase and prevents ethanol-induced liver injury through constitutive NOS dependent reduced redox signaling in ratsFood. Chem. Toxicol.59236-248(2013) 4.Arha, D., Pandeti, S., Mishra, A., et al.Deoxyandrographolide promotes glucose uptake through glucose transporter-4 translocation to plasma membrane in L6 myotubes and exerts antihyperglycemic effect in vivoEur. J. Pharmacol.768207-216(2015)
| Cas No. | 4176-97-0 | SDF | |
| 别名 | 14-去氧穿心莲内酯 | ||
| Canonical SMILES | O=C1OCC=C1CC[C@@H]2C(CC[C@]3([H])[C@](C)(CO)[C@H](O)CC[C@@]23C)=C | ||
| 分子式 | C20H30O4 | 分子量 | 334.45 |
| 溶解度 | Acetonitrile: soluble | 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 | 2.99 mL | 14.9499 mL | 29.8998 mL |
| 5 mM | 0.598 mL | 2.99 mL | 5.98 mL |
| 10 mM | 0.299 mL | 1.495 mL | 2.99 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。
14-Deoxyandrographolide alleviates ethanol-induced hepatosteatosis through stimulation of AMP-activated protein kinase activity in rats
Alcohol 2014 Mar;48(2):123-32.PMID:24507479DOI:10.1016/j.alcohol.2013.11.005.
Andrographis paniculata (AP) is a traditional medicinal plant of Ayurveda. It grows widely in Asia and is prescribed in the treatment of liver diseases. Here we have investigated the beneficial role of 14-Deoxyandrographolide (14-DAG), a bioactive diterpenoid from AP, against alcoholic steatosis in rats. 14-DAG was extracted from aerial parts (leaves and stems) of AP. Rats were fed with ethanol for 8 weeks. Animals were treated with 14-DAG during the last 4 weeks of ethanol treatment. In vitro studies were undertaken in a human hepatocellular liver carcinoma cell line culture. Hepatosteatosis was assessed from histopathological studies of liver sections. Acetyl-CoA, malonyl-CoA, and triglyceride contents were determined using commercially available kits. Fatty acid synthesis was evaluated from incorporation of 1-(14)C acetate. Regulation of fatty acid oxidation and lipogenesis were monitored with immunoblotting and immunoprecipitation studies. Ethanol exposure led to hepatotoxicity, as evident from the marked enhancement in the levels of AST and ALT. The values decreased almost to control levels in response to 14-DAG treatment. Results showed that ethanol feeding induced deactivation of AMP-activated protein kinase (AMPK) that led to enhanced lipid synthesis and decreased fatty acid oxidation, culminating in hepatic fat accumulation. Treatment with 14-DAG activated AMPK through induction of cyclic AMP-protein kinase A pathway. Activation of AMPK was followed by down-regulation of sterol regulatory element binding protein-1c, acetyl-CoA carboxylase, and fatty acid synthase, leading to suppression of lipogenesis. This was associated with up-regulation of sirtuin 1 and depletion of malonyl-CoA, in favor of increased fatty acid oxidation. 14-DAG controlled ethanol-induced hepatosteatosis by interfering with dysregulation of lipid metabolism. In conclusion, our results indicated that 14-DAG was capable of preventing the development of fatty liver through AMPK-mediated regulation of lipid metabolism. This finding supported the hepatoprotective role of 14-DAG, which might serve as a therapeutic option to alleviate hepatosteatosis in chronic alcoholism.
14-Deoxyandrographolide targets adenylate cyclase and prevents ethanol-induced liver injury through constitutive NOS dependent reduced redox signaling in rats
Food Chem Toxicol 2013 Sep;59:236-48.PMID:23764359DOI:10.1016/j.fct.2013.05.056.
Chronic alcoholism is one of the most common causes of liver diseases worldwide. Nitric oxide (NO) has been proposed to have potential for clinical application against chronic hepatocellular injuries. However, mechanisms underlying hepatoprotective functions of NO in ethanol-induced apoptosis are largely unknown. Sprauge-Dawley rats were exposed to ethanol for 8 weeks. Half of the ethanol-fed animals received 14-Deoxyandrographolide (14-DAG) treatment for the last 4 weeks of study. Preventive effect of 14-DAG against ethanol-induced hepatotoxicity involved constitutive nitric oxide synthase (cNOS) activation followed by up-regulation of γ-glutamylcysteine synthetase activity and reduced oxidative stress. Enhanced interaction of cNOS with caveolin-1 caused down-regulation of enzyme activity and led to depletion of NO in the hepatocytes of ethanol-fed animals. 14-DAG acted as activator of adenylate cyclase and modulated cyclic AMP (cAMP) mediated expression of caveolin-1 and calmodulin. This eventually favored activation of cNOS through inhibition of cNOS-caveolin-1 interaction. Our results suggest that, protective effect of 14-DAG against ethanol-induced hepatic injury is based on its ability to reduce oxidative stress through cNOS dependent improvement of redox status. 14-DAG mediated activation of adenylate cyclase-cAMP signaling leading to up-regulation of cNOS may provide a promising approach in the prevention of liver diseases during chronic alcoholism.
14-Deoxyandrographolide as a platelet activating factor antagonist in bovine neutrophils
Planta Med 2005 Jul;71(7):604-8.PMID:16041644DOI:10.1055/s-2005-871264.
14-Deoxyandrographolide (14-DAP) is a labdane diterpene isolated from Andrographis paniculata with previously reported calcium channel blocking activity. Its potential platelet activating factor (PAF) antagonistic activity in bovine neutrophils was assessed. 14-DAP, in concentrations between 10-100 microM, reduced the extracellular acidification rate and the intracellular alkalinization in a dose-dependent manner. In addition, 14-DAP reduced PAF-induced calcium flux in the presence of extracellular calcium, and tyrosine phosphorylation of a 44 kDa protein corresponding to the MAPK(ERK1). However, 14-DAP reduced the 3H-PAF binding with a Ki of 7.8 x 10 (- 9)M, and a Hill slope of 0.63, suggesting that there is more than one binding site for 14-DAP. We concluded that 14-DAP is an effective antagonist of PAF-mediated processes in bovine neutrophils, probably by virtue of its calcium channel blocking property.
Andrographis paniculata (Burm. F) Wall ex Nees: Antiviral properties
Phytother Res 2021 Oct;35(10):5365-5373.PMID:33929758DOI:10.1002/ptr.7145.
Andrographis paniculata is home to a rich variety of molecules especially andrographolide and its derivatives. Clinical properties of the andrographolide are multifarious and include: analgesic, antipyretic, antiretroviral, antiproliferative, antimalarial, antithrombotic, antihyperglycemic, antiurolethial, antilesihmaniasis, hepatoprotective, immune-modulatory, protective against alcohol induced toxicity and cardioproetcive activity and anticancer activity. Andrographolide, neoandrographolide, dehydroandrographolide and several natural and synthetic derivatives of it: 14-deoxy-11,12-didehydroandrographolide and 14-Deoxyandrographolide, dehydroandrographolide succinic acid monoester (DAMS), 14-ά-lipoyl andrographolide (AL-1), 14-acetyl-3,9-isopropyl-ideneandrographolide, 14-acetylandrographolide, 3,14,19-triacetylandrographolide, and 3,9-isopropyl-idene andrographolide, are shown to possess significant antiviral activity against HIV, influenza A, HBV, HCV, HPP and HSV. Studies on SARS CoV 2 is restricted to in silico molecular docking studies on viral targets and selected host target proteins. The main targets of andrographolide and its derivatives are fusion and adsorption of virus to the host cell, binding to viral receptor and co-receptor, enzymes involved in DNA/RNA/Genome replication by the virus, translation, post-translation and reverse transcription. Andrographolide as a drug is yet to reach its full therapeutic potential since this molecule shows low bioavailability. Andrographolide therapy is in need of an appropriate delivery system that may increase its bioavailability. Further high-quality studies are needed to firmly establish the clinical efficacy of the plant.
14-Deoxyandrographolide desensitizes hepatocytes to tumour necrosis factor-alpha-induced apoptosis through calcium-dependent tumour necrosis factor receptor superfamily member 1A release via the NO/cGMP pathway
Br J Pharmacol 2010 Aug;160(7):1823-43.PMID:20649583DOI:10.1111/j.1476-5381.2010.00836.x.
Background and purpose: Andrographis paniculata (AP) has been found to display hepatoprotective effect, although the mechanism of action of the active compounds of AP in this context still remains unclear. Here, we evaluated the hepatoprotective efficacy of 14-Deoxyandrographolide (14-DAG), a bioactive compound of AP, particularly its role in desensitization of hepatocytes to tumour necrosis factor-alpha (TNF-alpha)-induced signalling of apoptosis. Experimental approach: TNF-alpha-mediated ligand receptor interaction in hepatocytes in the presence of 14-DAG was studied in vitro in primary hepatocyte cultures, with the help of co-immunoprecipitation, confocal microscopy and FACS analysis. Events associated with 14-DAG-induced TNFRSF1A release from hepatocytes were determined using immunoblotting, biochemical assay and fluorimetric studies. Pulse-chase experiments with radiolabelled TNF-alpha and detection of apoptotic nuclei by terminal transferase-mediated dUTP nick-end labelling were performed under in vivo conditions. Key results: 14-DAG down-regulated the formation of death-inducing signalling complex, resulting in desensitization of hepatocytes to TNF-alpha-induced apoptosis. Pretreatment of hepatocytes with 14-DAG accentuated microsomal Ca-ATPase activity through induction of NO/cGMP pathway. This resulted in enhanced calcium influx into microsomal lumen with the formation of TNFRSF1A-ARTS-1-NUCB2 complex in cellular vesicles. It was followed by the release of full-length 55 kDa TNFRSF1A and a reduction in the number of cell surface TNFRSF1A, which eventually caused diminution of TNF-alpha signal in hepatocytes. Conclusion and implication: Taken together, the results demonstrate for the first time that 14-DAG desensitizes hepatocytes to TNF-alpha-mediated apoptosis through the release of TNFRSF1A. This can be used as a strategy against cytokine-mediated hepatocyte apoptosis in liver dysfunctions.