| Description: |
Oxyresveratrol , a dietary phenolic compound, has neuroprotective effect, as a potential nutritional candidate for protection against neurodegeneration in Parkinson disease; 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, it also as an antibrowning agent for cloudy apple juices and fresh-cut apples. Oxyresveratrol exhibits a potent inhibitory effect on dopa oxidase activity of tyrosinase which catalyzes rate-limiting steps of melanin biosynthesis.Oxyresveratrol exhibits the inhibitory activity at the early and late phase of viral replication and inhibited the viral replication with pretreatment in one-step growth assay of HSV-1 and HSV-2. |
| In vitro: |
| Free Radic Biol Med. 2008 Oct 1;45(7):1019-26. | | Dietary oxyresveratrol prevents parkinsonian mimetic 6-hydroxydopamine neurotoxicity.[Pubmed: 18675900 ] | Oxyresveratrol (OXY) is a polyhydroxylated stilbene existing in mulberry. Increasing lines of evidence have shown its neuroprotective effects against Alzheimer disease and stroke. However, little is known about its neuroprotective effect in Parkinson disease (PD).
Owing to its antioxidant activity, blood-brain barrier permeativity, and water solubility, we hypothesized that OXY may exert neuroprotective effects against parkinsonian mimetic 6-hydroxydopamine (6-OHDA) neurotoxicity.
METHODS AND RESULTS:
Neuroblastoma SH-SY5Y cells have long been used as dopaminergic neurons in PD research. We found that both pretreatment and posttreatment with OXY on SH-SY5Y cells significantly reduced the release of lactate dehydrogenase, the activity of caspase-3, and the generation of intracellular reactive oxygen species triggered by 6-OHDA. Compared to resveratrol, OXY exhibited a wider effective dosage range. We proved that OXY could penetrate the cell membrane by HPLC analysis of cell extracts. These results suggest that OXY may act as an intracellular antioxidant to reduce oxidative stress induced by 6-OHDA. Western blot analysis demonstrated that OXY markedly attenuated 6-OHDA-induced phosphorylation of JNK and c-Jun. Furthermore, we proved that OXY increased the basal levels of SIRT1, which may disclose new pathways accounting for the neuroprotective effects of OXY.
CONCLUSIONS:
Taken together, our results suggest OXY, a dietary phenolic compound, as a potential nutritional candidate for protection against neurodegeneration in PD. | | 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.
METHODS AND RESULTS:
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.
METHODS AND RESULTS:
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. | | J Agric Food Chem. 2007 Apr 4;55(7):2604-10. | | Oxyresveratrol as an antibrowning agent for cloudy apple juices and fresh-cut apples.[Pubmed: 17335224] | Antibrowning activities of Morus alba L. twig extracts, oxyresveratrol, and mulberroside A isolated from mulberry twig on cloudy apple juices and fresh-cut apple slices were evaluated by monitoring the change of a* value, total color difference (DeltaE), and visual observation.
METHODS AND RESULTS:
It was found, similar to 4-hexylresorcinol, that oxyresveratrol could effectively inhibit browning in cloudy apple juices at a concentration as low as 0.01% and that mulberry twig extract also showed remarkable antibrowning effects on cloudy apple juices. However, for fresh-cut apple slices, mulberry twig extract and oxyresveratrol needed to be used in combination at least with ascorbic acid to exhibit their antibrowning effects. Apple slice samples treated by dipping in a solution containing 0.001 M oxyresveratrol, 0.5 M isoascorbic acid, 0.05 M calcium chloride, and 0.025 M acetylcysteine did not undergo any substantial browning reaction for 28 days at 4 degrees C.
However mulberroside A did not show antibrowning effects on cloudy apple juices although it is also a good mushroom tyrosinase inhibitor. |
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| In vivo: |
| Chem Biol Interact. 2016 Feb 5;245:110-21. | | 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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
In conclusion, this study confirmed that oxyresveratrol protected hepatocytes against oxidative stress and mitochondrial dysfunction, which might be associated with activation of Nrf2. |
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