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14-Deoxyandrographolide
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name 14-Deoxyandrographolide
Price: $238 / 10mg
CAS No.: 4176-97-0
Catalog No.: CFN92802
Molecular Formula: C20H30O4
Molecular Weight: 334.45 g/mol
Purity: >=98%
Type of Compound: Diterpenoids
Physical Desc.: Powder
Source: The herbs of Andrographis paniculata (Burm. f.) Nees
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: 14-Deoxyandrographolide has hepatoprotective activity, mediates 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. It desensitizes hepatocytes to TNF-alpha-mediated apoptosis through the release of TNFRSF1A.
Targets: AMPK | NOS | cAMP | TNF-α | ATPase | Calcium Channel
In vitro:
Br J Pharmacol. 2010 Aug;160(7):1823-43.
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.[Pubmed: 20649583]
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.
METHODS AND RESULTS:
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. 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.
CONCLUSIONS:
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.
In vivo:
Food Chem Toxicol. 2013 Sep;59:236-48.
14-Deoxyandrographolide targets adenylate cyclase and prevents ethanol-induced liver injury through constitutive NOS dependent reduced redox signaling in rats.[Pubmed: 23764359]
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.
METHODS AND RESULTS:
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-Deoxyandrographolide against ethanol-induced hepatotoxicity involved constitutive nitric oxide synthase (cNOS) activation followed by up-regulation of γ-glutamylcysteine synthetase activity and reduced oxidative stress. 14-Deoxyandrographolide acted as activator of adenylate cyclase and modulated cyclic AMP (cAMP) mediated expression of caveolin-1 and calmodulin.
CONCLUSIONS:
Our results suggest that, protective effect of 14-Deoxyandrographolide against ethanol-induced hepatic injury is based on its ability to reduce oxidative stress through cNOS dependent improvement of redox status. 14-Deoxyandrographolide 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 Description
Source: The herbs of Andrographis paniculata (Burm. f.) Nees
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: 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.

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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.99 mL 14.9499 mL 29.8998 mL 59.7997 mL 74.7496 mL
5 mM 0.598 mL 2.99 mL 5.98 mL 11.9599 mL 14.9499 mL
10 mM 0.299 mL 1.495 mL 2.99 mL 5.98 mL 7.475 mL
50 mM 0.0598 mL 0.299 mL 0.598 mL 1.196 mL 1.495 mL
100 mM 0.0299 mL 0.1495 mL 0.299 mL 0.598 mL 0.7475 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Animal Research:
Alcohol. 2014 Mar;48(2):123-32.
14-Deoxyandrographolide alleviates ethanol-induced hepatosteatosis through stimulation of AMP-activated protein kinase activity in rats.[Pubmed: 24507479 ]
Here we have investigated the beneficial role of 14-Deoxyandrographolide (14-DAG), a bioactive diterpenoid from AP, against alcoholic steatosis in rats.
METHODS AND RESULTS:
14-Deoxyandrographolide was extracted from aerial parts (leaves and stems) of AP. Rats were fed with ethanol for 8 weeks. Animals were treated with 14-Deoxyandrographolide during the last 4 weeks of ethanol treatment.The values decreased almost to control levels in response to 14-Deoxyandrographolide treatment. Treatment with 14-Deoxyandrographolide 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-Deoxyandrographolide controlled ethanol-induced hepatosteatosis by interfering with dysregulation of lipid metabolism.
CONCLUSIONS:
In conclusion, our results indicated that 14-Deoxyandrographolide was capable of preventing the development of fatty liver through AMPK-mediated regulation of lipid metabolism. This finding supported the hepatoprotective role of 14-Deoxyandrographolide, which might serve as a therapeutic option to alleviate hepatosteatosis in chronic alcoholism.
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