|Source:||The herbs of Dracaena angustifolia|
|Biological Activity or Inhibitors:||1. Oxyresveratro can inhibit tyrosinase activity.
2. Oxyresveratro is useful to trauma models, as toxicity to glia could be beneficial by inhibiting reactive gliosis.
3. Oxyresveratrol has antioxidant activity, can reduce neuronal oxidative damage and protect hepatocytes against oxidative stress and mitochondrial dysfunction, which may be associated with activation of Nrf2.
|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: firstname.lastname@example.org
|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||4.095 mL||20.475 mL||40.95 mL||81.9001 mL||102.3751 mL|
|5 mM||0.819 mL||4.095 mL||8.19 mL||16.38 mL||20.475 mL|
|10 mM||0.4095 mL||2.0475 mL||4.095 mL||8.19 mL||10.2375 mL|
|50 mM||0.0819 mL||0.4095 mL||0.819 mL||1.638 mL||2.0475 mL|
|100 mM||0.041 mL||0.2048 mL||0.4095 mL||0.819 mL||1.0238 mL|
Arch Dermatol Res. 2014 Jul;306(5):475-87.
|Effects of resveratrol, oxyresveratrol, and their acetylated derivatives on cellular melanogenesis.[Pubmed: 24414332]|
|Resveratrol and Oxyresveratrol are naturally occurring phenolic compounds with various bioactivities, but their uses in cosmetics have been partly limited by their chemical instabilities. This study was performed to examine the anti-melanogenic effects of the acetylated derivatives from resveratrol and Oxyresveratrol. Resveratrol and Oxyresveratrol were chemically modified to triacetyl resveratrol and tetraacetyl Oxyresveratrol, respectively. The acetylated compounds were less susceptible than the parent compounds to oxidative discoloration. The acetylated compounds inhibited the activities of tyrosinases less than parent compounds in vitro, but they were as effective at cellular melanogenesis inhibition, indicating bioconversion to parent compounds inside cells. Supporting this notion, the parent compounds were regenerated when the acetylated compounds were digested with cell lysates. Although resveratrol and triacetyl resveratrol inhibited tyrosinase activity less effectively than Oxyresveratrol and tetraacetyl Oxyresveratrol in vitro, they inhibited cellular melanogenesis more effectively.|
J Sci Food Agric. 2014 Jul;94(9):1822-6.
|Fermentation of Smilax china root by Aspergillus usami and Saccharomyces cerevisiae promoted concentration of resveratrol and oxyresveratrol and the free-radical scavenging activity.[Pubmed: 24919869]|
|BACKGROUND: Smilax china root, which is rich in resveratrol and Oxyresveratrol, has been used as emergency foods as well as folk medicine. This study investigated changes in concentration of bioactive components and the free-radical scavenging capacity of Smilax china root during fermentation by Aspergillus usami and Saccharomyces cerevisiae. RESULTS: Resveratrol, Oxyresveratrol and piceid were quantified as major constituents in Smilax china root by using UPLC-ESI-MS. The concentration of Oxyresveratrol and resveratrol remarkably increased through fermentation and the transformation of piceid to resveratrol.|
Chem Biol Interact. 2015 Jun 20.
|Oxyresveratrol abrogates oxidative stress by activating ERK-Nrf2 pathway in the liver.[Pubmed: 26102008]|
|Oxyresveratrol is a polyphenolic phytoalexin produced by plants as an antioxidant. This study investigated the hepatoprotective effects of Oxyresveratrol as well as its underlying mechanism of action. Here, we evaluated the protective effects of Oxyresveratrol against tert-butyl hydroperoxide (tBHP)-induced severe oxidative stress in HepG2 cells as well as acute liver injury caused by carbon tetrachloride (CCl4) in mice. tBHP-induced reactive oxygen species production and cell death in hepatocytes were blocked by Oxyresveratrol, as indicated by MTT, TUNEL, and FACS analyses. Moreover, pretreatment with Oxyresveratrol increased nuclear translocation and transactivation of NF-E2-related factor 2 (Nrf2), as assessed by antioxidant response element reporter gene expression and immunofluorescence staining, and transactivated expression of both hemeoxygenase-1 and glutamate-cysteine ligase catalytic subunit. More importantly, Oxyresveratrol induced phosphorylation of Nrf2 mediated through activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Further, ERK inhibitors such as PD98059 and U0126 blocked phosphorylation of Nrf2 as well as the protective effect of Oxyresveratrol in mitochondria. In mice, oral administration of Oxyresveratrol significantly prevented hepatocyte degeneration, inflammatory cell infiltration, as well as elevation of plasma markers such as ALT and AST induced by CCl4 injection. In conclusion, this study confirmed that Oxyresveratrol protected hepatocytes against oxidative stress and mitochondrial dysfunction, which might be associated with activation of Nrf2.|
Free Radic Res. 2013 Mar;47(3):212-8.
|The protective effects of oxyresveratrol imine derivative against hydrogen peroxide-induced cell death in PC12 cells.[Pubmed: 23298159]|
|Oxyresveratrol (2',3,4',5-tetrahydroxystilbene) is a naturally occurring ingredient found in mulberries that shows potential as an antioxidant, anti-inflammatory, and neuroprotective agent. This study was performed to identify materials similar to Oxyresveratrol that may have more effective antioxidant properties. The cytoprotective effects of the imine analogs were greater than the effects of Oxyresveratrol and the other analogs at concentrations of 200 μM. The Compound 3, which is the most effective imine analog of Oxyresveratrol, exhibited these cytoprotective effects against hydrogen peroxide-induced oxidative stress through the regulation of heme oxygenase-1 (HO-1) expression and the translocation of nuclear factor E2-related factor 2 (Nrf2). Our results suggest that imine analogs of Oxyresveratrol may be useful agents in reducing neuronal oxidative damage.|
Eur J Pharmacol. 2012 Apr 5;680(1-3):55-62.
|Potential neuroprotective effects of oxyresveratrol against traumatic injury.[Pubmed: 22489319]|
|Oxyresveratrol is a potent antioxidant and free-radical scavenger found in mulberry wood (Morus alba L.) with demonstrated protective effects against cerebral ischemia. We analyzed the neuroprotective ability of Oxyresveratrol using an in vitro model of stretch-induced trauma in co-cultures of neurons and glia, or by exposing cultures to high levels of glutamate. Cultures were treated with 25 μM, 50 μM or 100 μM Oxyresveratrol at the time of injury. Trauma produced marked neuronal death when measured 24 h post-injury, and Oxyresveratrol significantly inhibited this death. Microscopic examination of glia suggested signs of toxicity in cultures treated with 100 μM Oxyresveratrol, as demonstrated by elevated S-100B protein release and a high proportion of cells with condensed nuclei. Cultures exposed to glutamate (100 μM) for 24 h exhibited ~ 37% neuronal loss, which was not inhibited by Oxyresveratrol. These results show that the two pathologies of high glutamate exposure and trauma are differentially affected by Oxyresveratrol treatment in vitro. Further studies using Oxyresveratrol in trauma models are warranted, as toxicity to glia could be beneficial by inhibiting reactive gliosis, which often occurs after trauma.|