stilbenes and Cerebral-Infarction

Dual-phase amyloid PET is considered a useful protocol to study patients with cognitive impairment. Early-phase 18F-florbetaben PET/CT has been proposed as a surrogate of 18F-FDG PET/CT providing information related to regional brain perfusion. We report the case of a 61-year-old woman referred to the cognitive impairment unit for study, preliminary diagnosed as probable Alzheimer disease. The dual-phase 18F-florbetaben PET/CT was shown as the main finding, no uptake in the left anterior thalamus. Memory and language symptoms have been described as primary clinical features of anterior thalamic infarctions that could be confused with the main manifestations of Alzheimer disease.

Topics: Alzheimer Disease; Aniline Compounds; Cerebral Infarction; Female; Humans; Middle Aged; Positron Emission Tomography Computed Tomography; Positron-Emission Tomography; Stilbenes

Oxidative stress and inflammation have been implicated in cerebral ischemia/reperfusion injury and complication of diabetes. The present study was designed to evaluate whether resveratrol has cerebroprotective action through antioxidant and anti-inflammatory actions in diabetic rats. Bilateral common carotid artery occlusion (30 min) and reperfusion (4 h) was employed to induce cerebral infarction in diabetic Wistar rats. Diabetes was induced by streptozocine (50 mg/kg) intraperitoneally at once. Diabetic animals were divided into groups as: normal, sham, ischemia-reperfusion, and resveratrol-treated (5, 10, 20, and 30 mg/kg). These were used for estimation of cerebral infarction. Furthermore, 20 mg/kg dose was selected for estimation of oxidative stress markers (malondialdehyde, superoxide dismutase, and catalase). Inflammatory markers like TNF-α, IL-6, IL-10, and myeloperoxidase were estimated and histological characters were studied. Resveratrol produced dose-dependent reduction in percent cerebral infarction. With resveratrol of 20 mg/kg dose, levels of oxidative stress markers and inflammatory markers like malondialdehyde, TNF-α, IL-6, and myeloperoxidase were reduced and there was a significant increase in the levels of antioxidant and anti-inflammatory markers like catalase, superoxide dismutase, and IL-10. In the present study, we found that mechanism(s) responsible for the cerebroprotective effect of resveratrol in the diabetic rat brain involves antioxidant and anti-inflammatory actions.

Topics: Animals; Anti-Inflammatory Agents; Antioxidants; Brain; Catalase; Cerebral Infarction; Cytokines; Diabetes Mellitus, Experimental; Malondialdehyde; Neuroprotective Agents; Oxidative Stress; Peroxidase; Rats; Rats, Wistar; Resveratrol; Stilbenes; Superoxide Dismutase

Oxidative stress and inflammation are two important pathological mechanisms involved in cerebral ischemia and reperfusion injury. In pathological conditions such as cerebral infarction, the free radical production is greater than that of elimination by endogenous anti-oxidant system, by this undesirable effect brain is highly injured. Resveratrol is reported to have anti-oxidant and anti-inflammatory, athero-protective activities. Therefore, the aim of the present study is to evaluate the therapeutic potential of resveratrol against cerebral infarction induced by ischemia and reperfusion injury in Wistar rats. Bi-common carotid occlusion followed by 4 h reperfusion model was used to induce cerebral infarction. Percent infarction, oxidative stress markers (malondialdehyde, catalase, superoxide dismutase) and inflammatory markers (myeloperoxidase, TNF-α, IL-6, ICAM-1 and IL-10) were measured. TNF-α, IL-6, IL-10, and intracellular adhesive molecule-I (ICAM-1) levels were quantified by enzyme-linked immunosorbent assay (ELISA). Resveratrol produced significant dose-dependent reduction in percent cerebral infarct volume. At resveratrol 20 mg/kg dose, there was a significant reduction in oxidative stress and inflammatory markers like malondialdehyde, TNF-α, IL-6, myeloperoxidase and ICAM-I and in contrast there was a significant increase in anti-oxidants and anti-inflammatory markers like superoxide dismutase, catalase and IL-10 levels. Resveratrol showed significant cerebroprotective action mediated by anti-oxidant and anti-inflammatory mechanisms.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Brain Ischemia; Cerebral Infarction; Male; Neuroprotective Agents; Oxidative Stress; Random Allocation; Rats; Rats, Wistar; Resveratrol; Stilbenes

Neuroprotective effects of parthenocissin A (PA), a novel antioxidant and free radical scavenger, were studied in a transient middle cerebral artery (MCA) occlusion model in rats for the first time. The animals were treated intraperitoneally with PA at 2.5, 5 or 10 mg/kg, for both 30 min before MCA occlusion and 6 h after reperfusion. The MCA was occluded for 1 h in anesthetized Sprague-Dawley rats. Compared with vehicle-treated controls, MCA occluded animals treated with PA showed dose-dependent reductions in brain infarction size with improved neurological and motor outcome. Biomedical assay showed that the PA treatment suppressed lipid peroxidation and restored superoxide dismutase (SOD) activity in brain tissue. In addition, the ischemia/reperfusion (I/R) induced elevation of nitric oxide (NO) production and nitric oxide synthase (NOS) activity in brain tissue was also inhibited. Thus, PA demonstrated a neuroprotective effect in the I/R model and the beneficial effects of the compound may result from the reduction of oxidative stress and the inhibition of NO production induced by I/R. The neuroprotective effects of PA have highlighted the potential use of stilbene oligomers in stroke therapy.

Topics: Animals; Brain; Brain Ischemia; Cerebral Infarction; Free Radical Scavengers; Indenes; Infarction, Middle Cerebral Artery; Lipid Peroxidation; Male; Molecular Structure; Neuroprotective Agents; Nitric Oxide; Nitric Oxide Synthase; Oxidative Stress; Rats; Reperfusion Injury; Resorcinols; Stilbenes; Superoxide Dismutase; Vitaceae

We investigated to what extent the antioxidative hydroxystilbene oxyresveratrol (trans-2,3',4,5'-tetrahydroxystilbene, OXY), that we showed earlier to be strongly neuroprotective in a stroke model, may cross the blood-brain barrier (BBB) in healthy rats and in subjects submitted to focal infarction. Tissue extraction and in vivo microdialysis in the striatum show that systematically applied OXY is able to penetrate the BBB in control animals, but to a low extent. Microdialysis samples from animals that were subjected to a middle cerebral artery occlusion (MCAO) displayed strongly increased OXY levels (more than six-fold) in the infarct region as compared to sham-operated rats. Our data show that OXY may exert direct protective effects in the brain by crossing the BBB and may prove an excellent complementary drug for the treatment of neurodegenerative disorders that causally involve oxidative/nitrosative stress, especially in stroke.

Topics: Animals; Area Under Curve; Blood-Brain Barrier; CD11b Antigen; Cerebral Infarction; Chromatography, High Pressure Liquid; Corpus Striatum; Fluorescein; Fluoresceins; Indoles; Infarction, Middle Cerebral Artery; Male; Microdialysis; Neuroprotective Agents; Organic Chemicals; Permeability; Rats; Reperfusion; Stilbenes; Time Factors; Tissue Distribution

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