trans-2-3--4-5--tetrahydroxystilbene and Disease-Models--Animal

Topics: Animals; Anti-Inflammatory Agents; Biomarkers; Colitis; Colon; Cytokines; Dextran Sulfate; Disease Models, Animal; Dose-Response Relationship, Drug; Gene Expression; Humans; Inflammation Mediators; Intestinal Mucosa; Nitric Oxide Synthase Type II; Organ Size; Plant Extracts; Rats; Spleen; Stilbenes

Oxyresveratrol and its glycoside are important natural active materials. As an effective tyrosine kinase inhibitor, oxyresveratrol may prevent herpes virus infection, inflammation and oxidative stress, as well as protect nerves. In addition, it is known to inhibit cell apoptosis following cerebral ischemia. In recent years, oxyresveratrol and its glycoside have been widely investigated, and their useful biological activities have been explored, indicating that they may be worthy of further comprehensive research. The aim of the present study was to evaluate the photoprotective effects of oxyresveratrol and its ability to abrogate inflammation and oxidative stress in a rat model of spinal cord injury (SCI). The authors identified that oxyresveratrol significantly reversed the SCI‑induced inhibition of Basso, Beattie, and Bresnahan scores, inhibited the SCI‑mediated increase in spinal cord water content, significantly suppressed SCI‑induced nuclear factor‑κB/p65, tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6 activities and reversed the malondialdehyde, superoxide dismutase, glutathione (GSH) and GSH peroxidase activities in SCI rats. SCI‑induced granulocyte‑macrophage colony‑stimulating factor (GM‑CSF), inducible nitric oxide synthase (iNOS) and cyclo‑oxygenase‑2 (COX‑2) protein expression was significantly suppressed by oxyresveratrol, and SCI‑mediated inhibition of nuclear factor (erythroid‑derived 2)‑like 2 (Nrf2) protein expression was significantly increased by oxyresveratrol. In conclusion, these results suggest that the effects of oxyresveratrol restores SCI, and abrogates inflammation and oxidative stress in rat model of SCI via the GM‑CSF, iNOS, COX‑2 and Nrf2 signaling pathway.

Topics: Animals; Antioxidants; Disease Models, Animal; Drug Administration Schedule; Female; Gene Expression Regulation; Glutathione Peroxidase; Granulocyte-Macrophage Colony-Stimulating Factor; Inflammation; Injections, Intraperitoneal; Interleukin-1beta; Interleukin-6; Locomotion; Malondialdehyde; Neuroprotective Agents; Nitric Oxide Synthase Type II; Oxidative Stress; Plant Extracts; Rats; Rats, Sprague-Dawley; Spinal Cord; Spinal Cord Injuries; Stilbenes; Superoxide Dismutase; Transcription Factor RelA; Tumor Necrosis Factor-alpha

Previous work has shown that the Smilacis chinae rhizome (SCR) markedly inhibits amyloid beta protein (25-35)-induced neuronal cell damage in cultured rat cortical neurons. The present study was conducted to further verify the neuroprotective effect of SCR on excitotoxic and cerebral ischemic injury using both in vitro and in vivo studies. Exposure of cultured cortical neurons to 1 mM N-methyl-D-aspartate (NMDA) for 12 h induced neuronal cell death. SCR (10 and 50 microg/ml) inhibited NMDA-induced neuronal death, elevation of intracellular calcium ([Ca(2+)](i)), and generation of reactive oxygen species (ROS) in primary cultures of rat cortical neurons. In vivo, SCR prevented cerebral ischemic injury induced by 3-h middle cerebral artery occlusion (MCAO) and 24-h reperfusion. The ischemic infarct was significantly reduced in rats that received SCR (30 and 50 mg/kg, orally), with a corresponding improvement in neurological function. Moreover, SCR treatment significantly decreased the histological changes observed following ischemia. Oxyresveratrol and resveratrol isolated from SCR also inhibited NMDA-induced neuronal death, increase in [Ca(2+)](i), and ROS generation in cultured cortical neurons, suggesting that the neuroprotective effect of SCR may be attributable to these compounds. Taken together, these results suggest that the neuroprotective effect of SCR against focal cerebral ischemic injury is due to its anti-excitotoxic effects and that SCR may have a therapeutic role in neurodegenerative diseases such as stroke.

Topics: Animals; Calcium; Cell Death; Cells, Cultured; Cerebral Cortex; Disease Models, Animal; Dose-Response Relationship, Drug; Excitatory Amino Acid Agonists; Infarction, Middle Cerebral Artery; Male; N-Methylaspartate; Neurons; Neuroprotective Agents; Plant Extracts; Plant Preparations; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Reperfusion Injury; Resveratrol; Rhizome; Smilax; Stilbenes; Time Factors

Oxidative stress is one of the major pathological factors in the cascade that leads to cell death in cerebral ischemia. Here, we investigated the neuroprotective effect of a naturally occurring antioxidant, oxyresveratrol, to reduce brain injury after cerebral stroke. We used the transient rat middle cerebral artery occlusion (MCAO) model of brain ischemia to induce a defined brain infarction. Oxyresveratrol was given twice intraperitoneally: immediately after occlusion and at the time of reperfusion. Oxyresveratrol (10 or 20 mg/kg) significantly reduced the brain infarct volume by approximately 54% and 63%, respectively, when compared to vehicle-treated MCAO rats. Also, the neurological deficits as assessed by different scoring methods improved in oxyresveratrol-treated MCAO rats. Histological analysis of apoptotic markers in the ischemic brain area revealed that oxyresveratrol treatment diminished cytochrome c release and decreased caspase-3 activation in MCAO rats. Also, staining for apoptotic DNA showed that the number of apoptotic nuclei in ischemic brain was reduced after oxyresveratrol treatment as compared to the vehicle-treated MCAO rats. This dose-dependent neuroprotective effect of oxyresveratrol in an in vivo stroke model demonstrates that this drug may prove to be beneficial for a therapeutic strategy to limit brain injury in acute brain ischemia.

Topics: Analysis of Variance; Animals; Brain Ischemia; Cell Death; Cerebral Cortex; Cerebral Infarction; Cytochromes c; Disease Models, Animal; DNA Fragmentation; Dose-Response Relationship, Drug; Epoprostenol; Immunohistochemistry; Infarction, Middle Cerebral Artery; Ischemic Attack, Transient; Male; Microtubule-Associated Proteins; Mitochondria; Neurologic Examination; Neurons; Neuroprotective Agents; Phosphopyruvate Hydratase; Plant Extracts; Rats; Rats, Wistar; Stilbenes; Time Factors

Fractionation of an ethyl acetate-soluble extract of the bark of Artocarpus dadah has led to the isolation of three new prenylated stilbenoid derivatives, 3-(gamma,gamma-dimethylallyl)resveratrol (1), 5-(gamma,gamma-dimethylallyl)oxyresveratrol (2), 3-(2,3-dihydroxy-3-methylbutyl)resveratrol (3), and a new benzofuran derivative, 3-(gamma,gamma-dimethylpropenyl)moracin M (4), along with six known compounds, oxyresveratrol, (+)-catechin, afzelechin-3-O-alpha-L-rhamnopyranoside, (-)-epiafzelechin, dihydromorin, and epiafzelechin-(4beta-->8)-epicatechin. From an ethyl acetate-soluble extract of the twigs of the same plant were isolated compound 4 and two new neolignan derivatives, dadahols A (5) and B (6), as well as 10 known compounds, oxyresveratrol, (+)-catechin, afzelechin-3-O-alpha-L-rhamnopyranoside, resveratrol, steppogenin, moracin M, isogemichalcone B, gemichalcone B, norartocarpetin, and engeletin. The structures of compounds 1-6 were determined using spectroscopic and chemical methods. Isolates were evaluated for their inhibitory effects against both cyclooxygenase-1 (COX-1) and -2 (COX-2) and in a mouse mammary organ culture assay.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Acetylation; Animals; Benzofurans; Breast; Catechin; Cell Transformation, Neoplastic; Chromatography, High Pressure Liquid; Chromatography, Thin Layer; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Disease Models, Animal; Indonesia; Isoenzymes; Membrane Proteins; Methylation; Mice; Mice, Inbred BALB C; Molecular Structure; Moraceae; Nuclear Magnetic Resonance, Biomolecular; Organ Culture Techniques; Plant Bark; Plant Extracts; Plant Shoots; Plants, Medicinal; Prostaglandin-Endoperoxide Synthases; Spectroscopy, Fourier Transform Infrared; Stereoisomerism; Stilbenes