|Source:||The herbs of Undaria pinnatifida|
|Biological Activity or Inhibitors:||1. Fucosterol has anti-diabetic activity in vivo, it exhibits an inhibition of sorbitol accumulations in the lenses and causes an inhibition of blood glucose level and glycogen degradation.
2. Fucosterol possesses anti-oxidant and hepatoprotective activities .
3. Fucosterol shows cytotoxic effect against breast and colon carcinoma cell lines.
4. Fucosterol exhibits anti-inflammatory activity which might attribute to inhibition of NO and ROS generation and suppression of the NF-κB pathway.
5. Fucosterol is a dual-LXR agonist that regulates the expression of key genes in cholesterol homeostasis in multiple cell lines without inducing hepatic triglyceride accumulation.
6. Fucosterol has antihistaminic, anticholinergic and antiviral activities.
7. Fucosterol could as an anti-obesity agent, it can inhibit expression of PPARγ and C/EBPα, resulting in a decrease of lipid accumulation in 3T3-L1 pre-adipocytes.
|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.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.4231 mL||12.1156 mL||24.2313 mL||48.4625 mL||60.5782 mL|
|5 mM||0.4846 mL||2.4231 mL||4.8463 mL||9.6925 mL||12.1156 mL|
|10 mM||0.2423 mL||1.2116 mL||2.4231 mL||4.8463 mL||6.0578 mL|
|50 mM||0.0485 mL||0.2423 mL||0.4846 mL||0.9693 mL||1.2116 mL|
|100 mM||0.0242 mL||0.1212 mL||0.2423 mL||0.4846 mL||0.6058 mL|
Arch Pharm Res. 2004 Nov;27(11):1120-2.
|Anti-diabetic activities of fucosterol from Pelvetia siliquosa.[Pubmed: 15595413]|
|Fucosterol isolated from Pelvetia siliquosa was tested for its anti-diabetic activity in vivo. Fucosterol, when administered orally at 30 mg/kg in streptozotocin-induced diabetic rats, was caused a significant decrease in serum glucose concentrations, and exhibited an inhibition of sorbitol accumulations in the lenses. Fucosterol, when administered orally at 300 mg/kg in epinephrine-induced diabetic rats, was also caused an inhibition of blood glucose level and glycogen degradation. These results demonstrated that Fucosterol is a main anti-diabetic principle from the marine algae P. siliquosa.|
Arch Pharm Res. 2003 Sep;26(9):719-22.
|Anti-oxidant activities of fucosterol from the marine algae Pelvetia siliquosa.[Pubmed: 14560919]|
|The anti-oxidant activities of Fucosterol isolated from the marine algae Pelvetia siliquosa were investigated. Fucosterol exhibited a significant decrease in serum transaminase activities elevated by hepatic damage induced by CCl4-intoxication in rats. Fucosterol inhibited the sGOT and sGPT activities by 25.57 and 63.16%, respectively. Fucosterol showed the increase in the anti-oxidant enzymes such as hepatic cytosolic superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH-px) activities by 33.89, 21.56 and 39.24%, respectively, in CCl4-intoxicated rats. These results suggest that Fucosterol possess not only the anti-oxidant, but also the hepatoprotective activities in rats.|
Pharmacogn Mag. 2012 Jan;8(29):60-4.
|Cytotoxicity of fucosterol containing fraction of marine algae against breast and colon carcinoma cell line.[Pubmed: 22438665]|
|Hexane fraction of Chondria dasyphylla (IC(50) 82.26 ± 4.09 μg/ml) and MeOH-H(2)O fraction of Ulva flexuosa (IC(50) 116.92 ± 8.58 μg/ml) showed cytotoxic activity against proliferation of T47D cells. Hexane fraction of Sargassum angustifolium was also observed for cytotoxicity against T47D and HT-29 cell lines (IC(50) 166.42 ± 26.7 and 190.24 ± 52.8 μg/ml), respectively. An investigation of a component from the hexane fraction of Sargassum angustifolium yielded a steroidal metabolite, Fucosterol, with cytotoxicity in T47D and HT29 (IC(50) 27.94 ± 9.3 and 70.41 ± 7.5 μg/ml). CONCLUSIONS: These results indicated that Fucosterol, the most abundant phytosterol in brown algae, is responsible for cytotoxic effect of this extract against breast and colon carcinoma cell lines.|
Food Chem Toxicol. 2013 Sep;59:199-206.
|Anti-inflammatory activity of edible brown alga Eisenia bicyclis and its constituents fucosterol and phlorotannins in LPS-stimulated RAW264.7 macrophages.[Pubmed: 23774261 ]|
|Although individual phlorotannins contained in the edible brown algae have been reported to possess strong anti-inflammatory activity, the responsible components of Eisenia bicyclis have yet to be fully studied. Thus, we evaluated their anti-inflammatory activity via inhibition against production of lipopolysaccharide (LPS)-induced nitric oxide (NO) and tert-butylhydroperoxide (t-BHP)-induced reactive oxygen species (ROS), along with suppression against expression of inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2), in RAW 264.7 cells. The anti-inflammatory activity potential of the methanolic extract and its fractions of E. bicyclis was in the order of dichloromethane>methanol>ethyl acetate>n-butanol. The strong anti-inflammatory dichloromethane fraction was further purified to yield Fucosterol. From the ethyl acetate fraction, six known phlorotannins were isolated: phloroglucinol, eckol, dieckol, 7-phloroeckol, phlorofucofuroeckol A and dioxinodehydroeckol. We found that these compounds, at non-toxic concentrations, dose-dependently inhibited LPS-induced NO production. Fucosterol also inhibited t-BHP-induced ROS generation and suppressed the expression of iNOS and COX-2. These results indicate that E. bicyclis and its constituents exhibited anti-inflammatory activity which might attribute to inhibition of NO and ROS generation and suppression of the NF-κB pathway and can therefore be considered as a useful therapeutic and preventive approach to various inflammatory and oxidative stress-related diseases.|
J Agric Food Chem. 2012 Nov 21;60(46):11567-75.
|Fucosterol is a selective liver X receptor modulator that regulates the expression of key genes in cholesterol homeostasis in macrophages, hepatocytes, and intestinal cells.[Pubmed: 23116181 ]|
|Fucosterol, a sterol that is abundant in marine algae, has hypocholesterolemic activity, but the mechanism underlying its effect is not clearly understood. Because data suggest that Fucosterol can increase plasma high-density lipoprotein concentrations, we investigated whether it could activate liver X receptors (LXRs), critical transcription factors in reverse cholesterol transport. Fucosterol dose-dependently stimulated the transcriptional activity of both LXR-α and -β in a reporter gene assay, responses that were attenuated by the LXR antagonist As(2)O(3). Fucosterol also activated co-activator recruitment in cell-free time-resolved fluorescence resonance energy transfer analysis. In THP-1-derived macrophages, it induced the transcriptional activation of ABCA1, ABCG1, and ApoE, key genes in reverse cholesterol transport, and thereby significantly increased the efflux of cholesterol. Fucosterol also regulated intestinal NPC1L1 and ABCA1 in Caco-2 cells. Notably, Fucosterol did not induce cellular triglyceride accumulation in HepG2 cells, primarily because of its upregulation of Insig-2a, which delays nuclear translocation of SREBP-1c, a key hepatic lipogenic transcription factor. These results suggest that Fucosterol is a dual-LXR agonist that regulates the expression of key genes in cholesterol homeostasis in multiple cell lines without inducing hepatic triglyceride accumulation.|
J Pharm Pharmacol. 2015 Aug;67(8):1170-8.
|Protective effect of fucosterol isolated from the edible brown algae, Ecklonia stolonifera and Eisenia bicyclis, on tert-butyl hydroperoxide- and tacrine-induced HepG2 cell injury.[Pubmed: 25773602 ]|
|Fucosterol is the primary sterol found in brown algae. Recently, considerable interest has been generated regarding Fucosterol due to its potential antioxidant, anti-inflammatory and antidiabetic effects. The aim of this study was to investigate the protective effects of Fucosterol on tert-butyl hydroperoxide (t-BHP)- and tacrine-induced oxidative stress in HepG2 cells. METHODS: Fucosterol by itself exhibited no cytotoxicity at concentrations below 100 μm by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay. The increased intracellular reactive oxygen species (ROS) and decreased glutathione levels observed in t-BHP- and tacrine-treated HepG2 cells were ameliorated by Fucosterol pretreatment, indicating that the protective effects of Fucosterol are mediated by the induction of cellular defence mechanisms against oxidative stress. Moreover, elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in tacrine-treated mice were significantly reduced after oral administration of Fucosterol. KEY FINDINGS: The hepatoprotective effects of Fucosterol may occur via an increase in the hepatic level of glutathione and a decrease in ROS production, thereby preventing hepatic damage and the resultant increases in ALT and AST activity. CONCLUSION: These results suggest that Fucosterol may be an effective hepatoprotective agent that could be useful for preventive therapies against oxidative stress-related hepatotoxicity.|
Pharmacologyonline, 2009, 1(1):1104-1112.
|Antihistaminic, Anticholinergic and Antiviral activities of Fucosterol from Turbinaria conoides (J.Agardh) Kutzing[Reference: WebLink]|
|Fucosterol (Stigmasta-5,24(28)-dien-3-ol) was isolated from cyclohexane extract of Turbinaria conoides (J.Agardh) Kutzing. The structure was identified by comparing with the reported physical and spectral data of the compound. The antihistaminic and anticholinergic activities have been evaluated using in vitro standard animal models in comparison to chlorpheniramine maleate and pancuronium respectively. Evaluation of the potency (EC50), affinity (pA2) of the Fucosterol and the maximal response (Emax) to the Histamine and acetylcholine were determined in the absence and presence of Fucosterol. Antiviral activity and cytotoxicity were performed in human embryonic lung, human epithelial and Vero cells. Fucosterol showed antiviral activity against tested viruses with EC50 values ranging from >4 μg/mL to >20 μg/mL in the cells. Fucosterol inhibited histamine (97%) and acetylcholine (94%) induced contractions at 20 μg/mL, which were comparable to that of 10 μg/mL of chlorpheniramine maleate and pancuronium respectively. Thus Fucosterol springs up to be potent antihistaminic and anticholinergic compound.|
Arch Pharm Res. 2014 Jun;37(6):713-20.
|Anti-adipogenic activity of the edible brown alga Ecklonia stolonifera and its constituent fucosterol in 3T3-L1 adipocytes.[Pubmed: 24014306 ]|
|Fucosterol is a sterol metabolite of brown algae and regulates genes involved with cholesterol homeostasis. As a part of our continuous search for anti-obesity agents from natural marine sources, the anti-adipogenic activities of Ecklonia stolonifera and its sterol, Fucosterol, were evaluated for the inhibition of adipocyte differentiation and lipid formation. Oil Red O staining was used to evaluate triglyceride contents in 3T3-L1 pre-adipocytes primed by differentiation medium (DM) I and DM II. The methanolic extract of E. stolonifera showed strong anti-adipogenic activity, and was thus fractionated with several solvents. Among the tested fractions, the dichloromethane (CH2Cl2) fraction was found to be the most active fraction, with significant inhibition (40.5 %) of intracellular lipid accumulation at a non-toxic concentration, followed by the ethyl acetate fraction (30.2 %) at the same concentration, while the n-butanol and water fractions did not show inhibitory activity within the tested concentrations. The strong anti-adipogenic CH2Cl2-soluble fraction was further purified by a repeated chromatography to yield Fucosterol. Fucosterol reduced lipid contents in a concentration-dependent manner without showing any cytotoxicity. Fucosterol treatment also yielded a decrease in the expression of the adipocyte marker proteins peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα) in a concentration-dependent manner. Taken together, these results suggest that Fucosterol inhibits expression of PPARγ and C/EBPα, resulting in a decrease of lipid accumulation in 3T3-L1 pre-adipocytes, indicating that the potential use of E. stolonifera and its bioactive Fucosterol as an anti-obesity agent.|