Blood-Brain-Barrier Disorders https://greenmedinfo.com/taxonomy/term/32308/all en Berberine attenuates experimental autoimmune encephalomyelitis in mice. https://greenmedinfo.com/article/berberine-attenuates-experimental-autoimmune-encephalomyelitis-mice PMID:  PLoS One. 2010;5(10):e13489. Epub 2010 Oct 19. PMID: 20976070 Abstract Title:  Berberine attenuates experimental autoimmune encephalomyelitis in C57 BL/6 mice. Abstract:  BACKGROUND: Berberine, an isoquinoline derivative alkaloid, has a wide range of pharmacological properties and is considered to have anti-inflammatory and neuroprotective effects. However, there are no reports about the effects and mechanisms of berberine in experimental autoimmune encephalomyelitis (EAE), an established model of multiple sclerosis (MS).METHODOLOGY/PRINCIPAL FINDINGS: Female C57 BL/6 mice immunized with myelin oligodendrocyte glycoprotein 35-55 amino acid peptide were treated with berberine at the day of disease onset and medication was administered daily until mice were sacrificed. Blood-brain barrier (BBB) permeability and the alteration of matrix metalloproteinase-2 (MMP-2, 72 kDa) and matrix metalloproteinase-9 (MMP-9, 92 kDa) in the brain and cerebrospinal fluid (CSF) of EAE mice were detected by quantitative measurement for Evan&#039;s blue (EB) content, Western blot and gelatin zymography respectively. The results showed that berberine attenuated clinical and pathological parameters of EAE, reduced the permeability of BBB, inhibited the activity and expression of MMP-9 but not MMP-2 in the CSF and brain of EAE mice.CONCLUSIONS/SIGNIFICANCE: These findings suggest that berberine is effective to attenuate the clinical severity of EAE in C57 BL/6 mice by reducing the permeability of BBB, decreasing the expression and activity of MMP-9, and decreasing the inflammatory infiltration. We think that berberine might be a potential therapeutic agent for MS. https://greenmedinfo.com/article/berberine-attenuates-experimental-autoimmune-encephalomyelitis-mice#comments Berberine Blood-Brain-Barrier Disorders Brain Inflammation Multiple Sclerosis Matrix metalloproteinase-2 (MMP-2) inhibitor Matrix metalloproteinase-9 (MMP-9) inhibitor Animal Study Wed, 29 Jun 2011 14:19:57 +0000 greenmedinfo 65040 at https://greenmedinfo.com Cocaine-induced blood-brain-barrier disruption may precipitate brain pathology. https://greenmedinfo.com/article/cocaine-induced-blood-brain-barrier-disruption-may-precipitate-brain-pathology PMID:  Int Rev Neurobiol. 2009;88:297-334. PMID: 19897082 Abstract Title:  Cocaine-induced breakdown of the blood-brain barrier and neurotoxicity. Abstract:  Role of cocaine in influencing blood-brain barrier (BBB) function is still unknown. Available evidences suggest that cocaine administration results in acute hyperthermia and alterations in brain serotonin metabolism. Since hyperthermia is capable to induce the breakdown of the BBB either directly or through altered serotonin metabolism, a possibility exists that cocaine may induce neurotoxicity by causing BBB disruption. This hypothesis is discussed in this review largely based on our own laboratory investigations. Our observations in rats demonstrate that cocaine depending on the dose and routes of administration induces profound hyperthermia, increased plasma and brain serotonin levels leading to BBB breakdown and brain edema formation. Furthermore, cocaine was able to enhance cellular stress as seen by upregulation of heat shock protein (HSP 72 kD) expression and resulted in marked neuronal and glial cell damages at the time of the BBB dysfunction. Taken together, these observations are the first to suggest that cocaine-induced BBB disruption is instrumental in precipitating brain pathology. The possible mechanisms of cocaine-induced BBB breakdown and neurotoxicity are discussed. https://greenmedinfo.com/article/cocaine-induced-blood-brain-barrier-disruption-may-precipitate-brain-pathology#comments Blood-Brain-Barrier Disorders Cocaine Toxicity Animal Study Tue, 27 Jul 2010 02:00:34 +0000 greenmedinfo 55776 at https://greenmedinfo.com Curcumin attenuates blood-brain barrier disruption after subarachnoid hemorrhage in mice. https://greenmedinfo.com/article/curcumin-attenuates-blood-brain-barrier-disruption-after-subarachnoid-hemorrha PMID:  J Surg Res. 2017 Jan ;207:85-91. Epub 2016 Sep 3. PMID: 27979493 Abstract Title:  Curcumin attenuates blood-brain barrier disruption after subarachnoid hemorrhage in mice. Abstract:  BACKGROUND: Early brain injury, one of the most important mechanisms underlying subarachnoid hemorrhage (SAH), comprises edema formation and blood-brain barrier (BBB) disruption. Curcumin, an active extract from the rhizomes of Curcuma longa, alleviates neuroinflammation by as yet unknown neuroprotective mechanisms. In this study, we examined whether curcumin treatment ameliorates SAH-induced brain edema and BBB permeability changes, as well as the mechanisms underlying this phenomenon.METHODS: We induced SAH in mice via endovascular perforation, administered curcumin 15 min after surgery and evaluated neurologic scores, brain water content, Evans blue extravasation, Western blot assay results, and immunohistochemical analysis results 24 h after surgery.RESULTS: Curcumin significantly improved neurologic scores and reduced brain water content in treated mice compared with SAH mice. Furthermore, curcumin decreased Evans blue extravasation, matrix metallopeptidase-9 expression, and the number of Iba-1-positive microglia in treated mice compared with SAH mice. At last, curcumin treatment increased the expression of the tight junction proteins zonula occludens-1 and occludin in treated mice compared with vehicle-treated and sample SAH mice.CONCLUSIONS: We demonstrated that curcumin inhibits microglial activation and matrix metallopeptidase-9 expression, thereby reducing brain edema and attenuating post-SAH BBB disruption in mice. <p><a href="https://greenmedinfo.com/article/curcumin-attenuates-blood-brain-barrier-disruption-after-subarachnoid-hemorrha" target="_blank">read more</a></p> https://greenmedinfo.com/article/curcumin-attenuates-blood-brain-barrier-disruption-after-subarachnoid-hemorrha#comments Aneurysmal subarachnoid hemorrhage (SAH) Blood-Brain-Barrier Disorders Curcumin Animal Study Sat, 17 Dec 2016 23:20:18 +0000 greenmedinfo 140632 at https://greenmedinfo.com Curcumin has a neuroprotective effect on focal cerebral ischemic rats by preventing blood-brain barrier damage. https://greenmedinfo.com/article/curcumin-has-neuroprotective-effect-focal-cerebral-ischemic-rats-preventing-bl PMID:  Chemotherapy. 2010;56(1):60-5. Epub 2010 Mar 19. PMID: 17303117 Abstract Title:  Neuroprotective effect of curcumin on focal cerebral ischemic rats by preventing blood-brain barrier damage. Abstract:  Curcumin, a member of the curcuminoid family of compounds, is a yellow colored phenolic pigment obtained from powdered rhizome of C. longa Linn. Recent studies have demonstrated that curcumin has protective effects against cerebral ischemia/reperfusion injury. However, little is known about its mechanism. Disruption of the blood-brain barrier occurs after stroke. Protection of the blood-brain barrier has become an important target of stroke interventions in experimental therapeutic. The objective of the present study was to determine whether curcumin prevents cerebral ischemia/reperfusion injury by protecting blood-brain barrier integrity. We report that a single injection of curcumin (1 and 2 mg/kg, i.v.) 30 min after focal cerebral ischemia/reperfusion in rats significantly diminished infarct volume, improved neurological deficit, decreased mortality, reduced the water content of the brain and the extravasation of Evans blue dye in ipsilateral hemisphere in a dose-dependent manner. In cultured astrocytes, curcumin significantly inhibited inducible nitric oxide synthase (iNOS) expression and NO(x) (Nitrites/nitrates contents) production induced by lipopolysaccharide (LPS)/tumor necrosis factor alpha (TNF(alpha)). Furthermore, curcumin prevented ONOO(-) donor SIN-1-induced cerebral capillaries endothelial cells damage. We concluded that curcumin ameliorates cerebral ischemia/reperfusion injury by preventing ONOO(-) mediated blood-brain barrier damage. https://greenmedinfo.com/article/curcumin-has-neuroprotective-effect-focal-cerebral-ischemic-rats-preventing-bl#comments Blood-Brain-Barrier Disorders Brain Ischemia Curcumin Lipopolysaccharide-Induced Toxicity Neuroprotective Agents Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Sat, 12 Feb 2011 12:48:55 +0000 greenmedinfo 61556 at https://greenmedinfo.com Duodenal and portal glucose changes shown to regulate eating behaviour via brain area modulations https://greenmedinfo.com/article/duodenal-and-portal-glucose-changes-shown-regulate-eating-behaviour-brain-area PMID:  J Neuroendocrinol. 2012 Apr 4. Epub 2012 Apr 4. PMID: 22487360 Abstract Title:  Brain processing of duodenal and portal glucose sensing. Abstract:  Peripheral and central glucose sensing play a major role in the regulation of food intake. Peripheral sensing occurs at duodenal and portal levels, but the importance of these sensing sites is still controversial. The aim of our study was to compare the respective influence of these sensing pathways on the eating patterns, plasma concentrations of glucose, insulin and GLP-1, as well as brain activity in juvenile pigs. In Experiment 1, we characterized the changes in the microstructure of a 30-min meal in 8 conscious animals after duodenal or portal glucose infusion in comparison to saline infusion. In Experiment 2, glucose, insulin and GLP-1 plasma concentrations were measured during 2h after duodenal or portal glucose infusions in 4 anesthetized animals. In Experiment 3, SPECT brain imaging was performed in 5 anesthetized animals receiving duodenal or portal glucose or saline infusions. Both duodenal and portal glucose decreased the amount of food consumed as well as the ingestion speed, but this effect appeared earlier with the portal infusion. Significant differences of glucose and GLP-1 plasma concentrations between treatments were found at the moment of brain imaging. Both duodenal and portal glucose infusions activated the dorsolateral prefrontal cortex and primary somatosensory cortex. Only duodenal glucose infusion induced the activation of the prepyriform area, orbitofrontal cortex, caudate and putamen, as well as the deactivation of the anterior prefrontal cortex and anterior entorhinal cortex, while only portal glucose infusion induced a significant activation of the insular cortex. We demonstrated that duodenal and portal glucose infusions led to the modulation of brain areas that are known to regulate eating behaviour, which probably explains the decrease of food intake after both stimulations. Though, these stimulation pathways induced specific systemic and central responses suggesting that different brain processing matrices are involved.© 2012 The Authors. Journal of Neuroendocrinology © 2012 Blackwell Publishing Ltd. https://greenmedinfo.com/article/duodenal-and-portal-glucose-changes-shown-regulate-eating-behaviour-brain-area#comments Blood-Brain-Barrier Disorders Eating Disorders Gut Brain Axis: Imbalance Brain-derived neurotrophic factor modulator Glucose Caudate Orbitofrontal Cortex Prepyriform Putamen Animal Study Sat, 14 Apr 2012 22:29:53 +0000 greenmedinfo 74326 at https://greenmedinfo.com Epstein-Barr virus can infect human Blood-Brain-Barrier cells contributing to multiple sclerosis pathogenesis. https://greenmedinfo.com/article/epstein-barr-virus-can-infect-human-blood-brain-barrier-cells-contributing-mul PMID:  J Neuroimmunol. 2011 Jan;230(1-2):173-7. Epub 2010 Sep 9. PMID: 20826008 Abstract Title:  Epstein-Barr virus infection of human brain microvessel endothelial cells: a novel role in multiple sclerosis. Abstract:  Multiple sclerosis (MS) is an inflammatory neurological disease that is widely regarded as the outcome of complex interactions between a genetic predisposition and an environmental trigger. Epstein-Barr virus (EBV) has recently been associated with the onset of MS, yet understanding how it elicits autoimmunity remains elusive. Neuroinflammation, including the entry of autoreactive T cells, likely follows a breach of the blood-brain barrier (BBB) leading to CNS lesions in MS. We show that EBV can infect human BBB cells leading to increased production of pro-inflammatory mediators that result in immune cell adherence thus modeling a key step in MS pathogenesis. https://greenmedinfo.com/article/epstein-barr-virus-can-infect-human-blood-brain-barrier-cells-contributing-mul#comments Blood-Brain-Barrier Disorders Epstein-Barr Virus Infections Multiple Sclerosis Epstein-Barr Virus Neurotoxic Diseases that are Linked Review Tue, 17 May 2011 03:11:00 +0000 greenmedinfo 63908 at https://greenmedinfo.com Fluoride may go through the blood-brain barrier and accumulate in rat hippocampus, and inhibit the activity of cholinesterase. https://greenmedinfo.com/article/fluoride-may-go-through-blood-brain-barrier-and-accumulate-rat-hippocampus-and PMID:  Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2003 Apr ;21(2):102-4. PMID: 14761523 Abstract Title:  [Studies on fluoride concentration and cholinesterase activity in rat hippocampus]. Abstract:  OBJECTIVE: To study the accumulation of fluoride in rat hippocampus and its effect on cholinesterase activity.METHODS: Rats were subchronically exposed to NaF, and fluoride concentration and cholinesterase activity in rat hippocampus were determined.RESULTS: Fluoride concentration in rat hippocampus was significantly correlated with the dosage of fluoride, and there were significant differences among high dosage group [(13.03 +/- 1.79) micro g/g], low dosage group [(9.83 +/- 0.92) micro g/g] and control [(8.27 +/- 1.11) micro g/g], P<p><a href="https://greenmedinfo.com/article/fluoride-may-go-through-blood-brain-barrier-and-accumulate-rat-hippocampus-and" target="_blank">read more</a></p> https://greenmedinfo.com/article/fluoride-may-go-through-blood-brain-barrier-and-accumulate-rat-hippocampus-and#comments Blood-Brain-Barrier Disorders Brain Injury: Hippocampal Damage Acetylcholinesterase inhibitor (xenobiotic) Fluoride Neurotoxic Animal Study Wed, 14 Feb 2024 16:03:01 +0000 greenmedinfo 288445 at https://greenmedinfo.com High vitamin C supplementation reduces amyloid plaque deposition, blood brain barrier disruptions and mitochondrial dysfunction in the brains of 5XFAD mice. https://greenmedinfo.com/article/high-vitamin-c-supplementation-reduces-amyloid-plaque-deposition-blood-brain-b PMID:  Cell Death Dis. 2014 ;5:e1083. Epub 2014 Feb 27. PMID: 24577081 Abstract Title:  High-dose of vitamin C supplementation reduces amyloid plaque burden and ameliorates pathological changes in the brain of 5XFAD mice. Abstract:  Blood-brain barrier (BBB) breakdown and mitochondrial dysfunction have been implicated in the pathogenesis of Alzheimer&#039;s disease (AD), a neurodegenerative disease characterized by cognitive deficits and neuronal loss. Besides vitamin C being as one of the important antioxidants, recently, it has also been reported as a modulator of BBB integrity and mitochondria morphology. Plasma levels of vitamin C are decreased in AD patients, which can affect disease progression. However, investigation using animal models on the role of vitamin C in the AD pathogenesis has been hampered because rodents produce with no dependence on external supply. Therefore, to identify the pathogenic importance of vitamin C in an AD mouse model, we cross-bred 5 familial Alzheimer&#039;s disease mutation (5XFAD) mice (AD mouse model) withι-gulono-γ-lactone oxidase (Gulo) knockout (KO) mice, which are unable to synthesize their own vitamin C, and produced Gulo KO mice with 5XFAD mice background (KO-Tg). These mice were maintained on either low (0.66 g/l) or high (3.3 g/l) supplementation of vitamin C. We found that the higher supplementation of vitamin C had reduced amyloid plaque burden in the cortex and hippocampus in KO-Tg mice, resulting in amelioration of BBB disruption and mitochondrial alteration. These results suggest that intake of a larger amount of vitamin C could be protective against AD-like pathologies. https://greenmedinfo.com/article/high-vitamin-c-supplementation-reduces-amyloid-plaque-deposition-blood-brain-b#comments Alzheimer's Disease Blood-Brain-Barrier Disorders Vitamin C Antioxidants Neuroprotective Agents Mitochondrial Metabolism Transgenic Animal Study Animal Study Wed, 01 Jul 2015 18:47:35 +0000 greenmedinfo 118619 at https://greenmedinfo.com Magnesium sulfate attenuates increased blood-brain barrier permeability during insulin-induced hypoglycemia in rats. https://greenmedinfo.com/article/magnesium-sulfate-attenuates-increased-blood-brain-barrier-permeability-during PMID:  Can J Physiol Pharmacol. 2001 Sep;79(9):793-8. PMID: 11599780 Abstract Title:  Magnesium sulfate attenuates increased blood-brain barrier permeability during insulin-induced hypoglycemia in rats. Abstract:  Magnesium probably protects brain tissue against the effects of cerebral ischemia, brain injury and stroke through its actions as a calcium antagonist and inhibitor of excitatory amino acids. The effects of magnesium sulfate on cerebrovascular permeability to a dye, Evans blue, were studied during insulin-induced hypoglycemia with hypothermia in rats. Hypoglycemia was induced by an intramuscular injection of insulin. After giving insulin, each animal received MgSO4 (270 mg/kg) ip, followed by a 27 mg/kg dose every 20 min for 2.5 h. Plasma glucose and Mg2+ levels of animals were measured. Magnesium concentrations increased in the serum following MgSO4 administration (6.05+/-0.57 vs. 2.58+/-0.14 mg/dL in the Mg2+ group, and 7.14+/-0.42 vs. 2.78+/-0.06 mg/dL in the insulin + Mg2+ group, P https://greenmedinfo.com/article/magnesium-sulfate-attenuates-increased-blood-brain-barrier-permeability-during#comments Blood-Brain-Barrier Disorders Hyperinsulinism Hypoglycemia Magnesium Animal Study Wed, 13 Oct 2010 22:18:27 +0000 greenmedinfo 57703 at https://greenmedinfo.com Polystyrene nanoparticles are capable of entering through the blood-brain-barrier in an animal model of brain ischemia and perfusion. https://greenmedinfo.com/article/polystyrene-nanoparticles-are-capable-entering-through-blood-brain-barrier-ani PMID:  Anal Chem. 2004 Aug 1 ;76(15):4465-71. PMID: 15283589 Abstract Title:  Nanoparticle-based in vivo investigation on blood-brain barrier permeability following ischemia and reperfusion. Abstract:  The blood-brain barrier (BBB) represents a significant impediment to a large variety of central nervous system-active agents. In the current study, we applied fluorescent polystyrene nanospheres (20 nm) to study the BBB permeability following cerebral ischemia and reperfusion. A microdialysis probe was implanted in the cerebral cortex of an anesthetized rat injected with fluorescent polystyrene nanospheres. The circulating nanospheres extravasating to the brain extracellular fluids were collected by the probe. Fluorescence intensity in the microdialysates throughout the course of cerebral ischemia/reperfusion was measured. Cerebral ischemia and reperfusion induced transient accumulations of extracellular nanospheres in the brain. The accumulation of nanospheres may result from their extravasation from the blood vessels. The concurrent cerebral oxygen levels monitored using oxygen-dependent quenching of phosphorescence decreased following ischemia and returned to their original levels after reperfusion. In conclusion, we demonstrated that high temporal resolution measurements of BBB permeability in vivo can be obtained using fluorescence polystyrene nanospheres and that these data correlate with changes of cerebral oxygen concentration. This present investigation indicates that nanoparticles have potential clinical applications involving drug delivery and determination of therapeutic efficacy and on-site diagnosis. https://greenmedinfo.com/article/polystyrene-nanoparticles-are-capable-entering-through-blood-brain-barrier-ani#comments Blood-Brain-Barrier Disorders Nanotechnology Polystyrene nanoparticles Animal Study Sun, 15 Apr 2012 14:09:36 +0000 greenmedinfo 74334 at https://greenmedinfo.com Resveratrol attenuates oxidized LDL-evoked adverse changes in cerebrovascular endothelial cells. https://greenmedinfo.com/article/resveratrol-attenuates-oxidized-ldl-evoked-adverse-changes-cerebrovascular-end PMID:  J Cereb Blood Flow Metab. 2011 Mar;31(3):842-54. Epub 2010 Oct 13. PMID: 20940732 Abstract Title:  Resveratrol attenuates oxidized LDL-evoked Lox-1 signaling and consequently protects against apoptotic insults to cerebrovascular endothelial cells. Abstract:  Cerebrovascular endothelial cells (CECs) are crucial components of the blood-brain barrier. Our previous study showed that oxidized low-density lipoprotein (oxLDL) induces apoptosis of CECs. This study was designed to further evaluate the effects of resveratrol on oxLDL-induced CEC insults and its possible molecular mechanisms. Resveratrol decreased the oxidation of LDL into oxLDL. Additionally, the oxLDL-caused oxidative stress and cell damage were attenuated by resveratrol. Exposure of CECs to oxLDL induced cell shrinkage, DNA fragmentation, and cell apoptosis, but resveratrol defended against such injuries. Application of Lox-1 small interference (si)RNA into CECs reduced the translation of this membrane receptor, and simultaneously increased resveratrol protection from oxLDL-induced cell apoptosis. By comparison, overexpression of Lox-1 attenuated resveratrol protection. Resveratrol inhibited oxLDL-induced Lox-1 mRNA and protein expressions. Both resveratrol and Lox-1 siRNA decreased oxLDL-enhanced translocation of proapoptotic Bcl-2-associated X protein (Bax) from the cytoplasm to mitochondria. Sequentially, oxLDL-induced alterations in the mitochondrial membrane potential, cytochrome c release, and activities of caspases-9, -3, and -6 were decreased by resveratrol. Pretreatment with Z-VEID-FMK (benzyloxycarbonyl-Leu-Glu-His-Asp-fluoromethyl ketone) synergistically promoted resveratrol&#039;s protection against DNA fragmentation and cell apoptosis. Therefore, this study shows that resveratrol can protect CECs from oxLDL-induced apoptotic insults via downregulating Lox-1-mediated activation of the Bax-mitochondria-cytochrome c-caspase protease pathway. https://greenmedinfo.com/article/resveratrol-attenuates-oxidized-ldl-evoked-adverse-changes-cerebrovascular-end#comments Blood-Brain-Barrier Disorders Cholesterol: Oxidation Resveratrol Neuroprotective Agents In Vitro Study Thu, 10 Mar 2011 23:29:19 +0000 greenmedinfo 62491 at https://greenmedinfo.com Resveratrol protects against oxidized LDL-induced breakage of the blood-brain barrier. https://greenmedinfo.com/article/resveratrol-protects-against-oxidized-ldl-induced-breakage-blood-brain-barrier PMID:  J Nutr. 2010 Dec;140(12):2187-92. Epub 2010 Oct 27. PMID: 20980646 Abstract Title:  Resveratrol protects against oxidized LDL-induced breakage of the blood-brain barrier by lessening disruption of tight junctions and apoptotic insults to mouse cerebrovascular endothelial cells. Abstract:  Cerebrovascular endothelial cells (CEC) comprise the blood-brain barrier (BBB). In a previous study, we showed that oxidized LDL (oxLDL) can induce apoptosis of mouse CEC. Resveratrol possesses chemopreventive potential. This study aimed to evaluate the effects of resveratrol on oxLDL-induced insults to mouse CEC and its possible mechanisms. Exposure of mouse CEC to 200μmol/L oxLDL for 1 h did not cause cell death but significantly altered the permeability and transendothelial electrical resistance of the cell monolayer. However, resveratrol completely normalized such injury. As for the mechanisms, resveratrol completely protected oxLDL-induced disruption of F-actin and microtubule cytoskeletons as well as occludin and zona occludens-1 (ZO-1) tight junctions. The oxLDL-induced decreases in the mitochondrial membrane potential and intracellular ATP levels were normalized by resveratrol. Exposure of mouse CEC to 200 μmol/L oxLDL for 24 h elevated oxidative stress and simultaneously induced cell apoptosis. However, resveratrol partially protected against oxLDL-induced CEC apoptosis. The oxLDL-induced alterations in levels of Bcl-2, Bax, and cytochrome c were completely normalized by resveratrol. Consequently, resveratrol partially decreased oxLDL-induced activation of caspases-9 and -3. Therefore, in this study, we show that resveratrol can protect against oxLDL-induced damage of the BBB through protecting disruption of the tight junction structure and apoptotic insults to CEC. https://greenmedinfo.com/article/resveratrol-protects-against-oxidized-ldl-induced-breakage-blood-brain-barrier#comments Blood-Brain-Barrier Disorders Cholesterol: Oxidation Endothelial Dysfunction Resveratrol Antioxidants Neuroprotective Agents Stilbenes Animal Study Thu, 10 Mar 2011 23:01:54 +0000 greenmedinfo 62477 at https://greenmedinfo.com Sesamol improves blood-brain-barrier function in diabetic rats. https://greenmedinfo.com/article/sesamol-improves-blood-brain-barrier-function-diabetic-rats PMID:  Exp Brain Res. 2009 Jul ;197(1):23-34. Epub 2009 Jun 30. PMID: 19565232 Abstract Title:  Administration of sesamol improved blood-brain barrier function in streptozotocin-induced diabetic rats. Abstract:  Uncontrolled or poorly controlled blood glucose during diabetes is an important factor in worsened vascular function. While evidence suggests that hyperglycemia-induced oxidative stress plays a prominent role in development of microangiopathy of the retina, kidney, and nerves, the role oxidative stress plays on blood-brain barrier (BBB) function and structure has lagged behind. In this study, a natural antioxidant, sesamol, was administered to streptozotocin (STZ)-induced diabetic rats to examine the role that oxidative stress plays on BBB structure and function. Experiments were conducted at 56 days after STZ injection. Male Sprague-Dawley rats randomly were divided into four treatment groups CON--control; STZ--STZ-induced diabetes; CON + S--control + sesamol; STZ + S--STZ-induced diabetes + sesamol. Functional and structural changes to the BBB were measured by in situ brain perfusion and western blot analysis of changes in tight junction protein expression. Oxidative stress markers were visualized by fluorescent confocal microscopy and assayed by spectrophotometric analysis. Results demonstrated that the increased BBB permeability observed in STZ-induced diabetic rats was attenuated in STZ + S rats to levels observed in CON. Sesamol treatment reduced the negative impact of STZ-induced diabetes on tight junction protein expression in isolated cerebral microvessels. Oxidative stress markers were elevated in STZ as compared to CON. STZ + S displayed an improved antioxidant capacity which led to a reduced expression of superoxide and peroxynitrite and reduced lipid peroxidation. In conclusion, this study showed that sesamol treatment enhanced antioxidant capacity of the diabetic brain and led to decreased perturbation of hyperglycemia-induced changes in BBB structure and function. https://greenmedinfo.com/article/sesamol-improves-blood-brain-barrier-function-diabetic-rats#comments Blood-Brain-Barrier Disorders Diabetes: Cognitive Dysfunction Oxidative Stress Sesamol Antioxidants Transgenic Animal Study Fri, 16 Sep 2011 21:21:59 +0000 greenmedinfo 68638 at https://greenmedinfo.com Some statin drugs are may cause neurological problems due to their ability to cross the blood-brain barrier. https://greenmedinfo.com/article/some-statin-drugs-are-may-cause-neurological-problems-due-their-ability-cross- PMID:  Pharm Res. 1994 Feb ;11(2):305-11. PMID: 8165193 Abstract Title:  In vivo and in vitro blood-brain barrier transport of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors. Abstract:  Among the HMG-CoA reductase inhibitors, lovastatin and simvastatin have central nervous system (CNS) side effects, such as sleep disturbance, whereas pravastatin does not. This difference in CNS side effects may be due to a difference in blood-brain barrier (BBB) permeability among these inhibitors. To test this hypothesis, we compared the BBB transport ability of HMG-CoA reductase inhibitors by using an in vivo brain perfusion technique in rats and an in vitro culture system of bovine brain capillary endothelial cells. The in vivo BBB permeability coefficients of the lipophilic inhibitors, [14C]lovastatin and [14C]simvastatin, were high. In contrast, that of the hydrophilic inhibitor, [14C]pravastatin, was low and not significantly different from that of [14C]sucrose, an extracellular space marker. Similarly, the in vitro BBB permeability coefficients of [14C]lovastatin and [1C]simvastatin were high, while that of [14C]-pravastatin was low. The in vivo and in vitro transcellular permeabilities obtained for HMG-CoA reductase inhibitors were comparable. This study shows that the BBB permeability correlates with the CNS side effects of the HMG-CoA reductase inhibitors. https://greenmedinfo.com/article/some-statin-drugs-are-may-cause-neurological-problems-due-their-ability-cross-#comments Blood-Brain-Barrier Disorders Statin-Induced Pathologies Lovastatin Neurotoxic Simvastatin Statin Drugs Animal Study Sun, 13 Nov 2011 01:41:16 +0000 greenmedinfo 69796 at https://greenmedinfo.com Sulforaphane improves cognitive function administered following traumatic brain injury. https://greenmedinfo.com/article/sulforaphane-improves-cognitive-function-administered-following-traumatic-brai PMID:  Neurosci Lett. 2009 Aug 28;460(2):103-7. Epub 2009 Apr 15. PMID: 19515491 Abstract Title:  Sulforaphane improves cognitive function administered following traumatic brain injury. Abstract:  Recent studies have shown that sulforaphane, a naturally occurring compound that is found in cruciferous vegetables, offers cellular protection in several models of brain injury. When administered following traumatic brain injury (TBI), sulforaphane has been demonstrated to attenuate blood-brain barrier permeability and reduce cerebral edema. These beneficial effects of sulforaphane have been shown to involve induction of a group of cytoprotective, Nrf2-driven genes, whose protein products include free radical scavenging and detoxifying enzymes. However, the influence of sulforaphane on post-injury cognitive deficits has not been examined. In this study, we examined if sulforaphane, when administered following cortical impact injury, can improve the performance of rats tested in hippocampal- and prefrontal cortex-dependent tasks. Our results indicate that sulforaphane treatment improves performance in the Morris water maze task (as indicated by decreased latencies during learning and platform localization during a probe trial) and reduces working memory dysfunction (tested using the delayed match-to-place task). These behavioral improvements were only observed when the treatment was initiated 1h, but not 6h, post-injury. These studies support the use of sulforaphane in the treatment of TBI, and extend the previously observed protective effects to include enhanced cognition. https://greenmedinfo.com/article/sulforaphane-improves-cognitive-function-administered-following-traumatic-brai#comments Blood-Brain-Barrier Disorders Brain Damage Brain Injury: Traumatic Cognitive Decline/Dysfunction Sulforaphane Anticarcinogenic Agents Neuroprotective Agents Animal Study Tue, 26 Oct 2010 23:58:36 +0000 greenmedinfo 58045 at https://greenmedinfo.com