Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied some hemodynamic parameters as heart rate (HR) developed pressure (DP) and maximal positive values of the first derivative of pressure (+dP/dt max) in isolated heart from control or resveratrol treated rats. In acute ex vivo experiments, resveratrol (1-100 microM) infusion in Langendorff perfused hearts did not affect contractile function in either normoxic conditions or after ischemia/reperfusion. However when semi-chronically administered by IP injection during 7 days, resveratrol which had no effect on pre-ischemic heart greatly improved post-ischemic indexes of myocardial function. Resveratrol effect is dose-dependent and seemed optimal at a plasma level of 18.5 microM. This concentration is very close to that previously shown to be optimal and non-toxic by others. These beneficial effects of resveratrol are only partly explained by its antioxidant properties as suggested by the lack of any dose-response effect on tissue malondialdehyde (MDA) levels. They are also clearly not mediated by nitric oxide (NO) elevation. When acutely infused resveratrol had no beneficial effect and therefore could not be proposed in acute scenarios of ischemia/reperfusion or stroke. However resveratrol appeared as an efficient and promising molecule in the prevention of heart dysfunction.
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PMID:Strong cardioprotective effect of resveratrol, a red wine polyphenol, on isolated rat hearts after ischemia/reperfusion injury. 1712 27

trans-Resveratrol (RSV) has been shown to have cardioprotective effect during ischemia-reperfusion through reactive oxygen species (ROS)-scavenging activity. Elevated ROS has been implicated in the initiation and progression of atherosclerosis. The nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a major source of vascular ROS formation. In the present study, we show that exposure of vascular endothelial cells (EC) to oxidized low-density lipoproteins (oxLDL) results in elevations of NOX activity and cellular ROS levels. The oxLDL effects are effectively suppressed by RSV or astringinin (AST), either before or after oxLDL exposure. In this study, we show that RSV or AST treatment appears to suppress NOX activity by reducing the membrane association of gp91(phox) and Rac1, two protein species required for the assembly of active NOX complex. Exposure to RSV or AST protects EC from oxidative functional damages, including antiplatelet activity and mononucleocyte adhesion. In addition, ANG II-induced NOX activation is also attenuated. These results suggest that RSV or AST protects EC from oxLDL-induced oxidative stress by both direct ROS scavenging and inhibition of NOX activity.
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PMID:Resveratrol attenuates oxLDL-stimulated NADPH oxidase activity and protects endothelial cells from oxidative functional damages. 1719 32

Resveratrol (trans-3,4',5-trihydroxystilbene) is a natural phytoalexin found in grape skin, and has been suggested to be an antioxidant agent, an anticancer agent and a cardioprotective agent. In particular, recent experimental evidence has demonstrated that resveratrol exhibits neuroprotective effects in various assay systems. During the study on the resveratrol derivatives, we found that (4-methoxybenzylidene)-(3-methoxyphenyl)amine (MBMPA), which has blocked free phenolic groups, strongly protects neuronal cells against ischemic damage on a higher activity than resveratrol. The MBMPA potently reduced the level of neuronal cell death in an oxygen and glucose deprivation-exposed rat organotypic hippocampal slice culture. In addition, ATP depletion following the onset of oxygen and glucose deprivation in an adult hippocampal slice was blocked by the MBMPA treatment. These results suggest that MBMPA has a neuroprotective effect on an in vitro ischemia model, and may be useful for treating stroke.
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PMID:Protective effect of (4-methoxybenzylidene)-(3-methoxynophenyl)amine against neuronal cell death induced by oxygen and glucose deprivation in rat organotypic hippocampal slice culture. 1720 85

Resveratrol (trans-3,4',5-trihydroxystilbene, CAS 501-36-0), a natural antioxidant and polyphenol found in grapes and wine, has been found to pharmacologically precondition the heart in nitric oxide (NO)-dependent manner. In the vascular system, NO functions as an endogenous inhibitor of leukocyte chemotaxis, adherence, and activation. The present study was designed to determine if resveratrol, through NO, can block the proadhesive molecules generated in the ischemic reperfused myocardium. Isolated hearts were prepared from properly anesthetized rats, and mounted on a Langendorff apparatus. The hearts were randomly assigned to one of the three groups: (i) control, (ii) resveratrol, and (iii) resveratrol + NG-nitro-L-arginine ethyl ester (L-NAME). The hearts were perfused in the absence (n = 6) or presence of 10 micromol/L resveratrol (n=6) or resveratrol + L-NAME (n = 6) for 15 min. All the hearts were then subjected to 30 min ischemia followed by 2 h of reperfusion. Ventricular function was monitored, infarct size and apoptotic cell death measured, and the proadhesive molecules and malonaldehyde formation determined in the perfusate. Resveratrol significantly improved postischemic ventricular function and reduced myocardial infarct size compared to the non-treated control group. The amount of proadhesive molecules including soluble intracellular adhesion molecule-1 (sICAM-1), endothelial leukocyte adhesion molecule-1 (sE-Selectin) and vascular cell adhesion molecule-1 (sVCAM-1) were each significantly decreased during reperfusion in the resveratrol group. L-NAME, a NO blocker, completely abolished such beneficial effects of resveratrol. The results support an anti-inflammatory action of resveratrol through a NO-dependent mechanism.
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PMID:Attenuation of ischemia/reperfusion injury in rats by the anti-inflammatory action of resveratrol. 1722 66

Resveratrol, a natural polyphenol, has a variety of effects including protection against ischemia-reperfusion injury, and antitumor and chemopreventive action against malignant tumors. In recent years, resveratrol has been found to exert pro-and anti-angiogenic effects, depending on the situation. For example, pro-angiogenic effects are noted in the peri-infarct myocardium, whereas resveratrol inhibits angiogenesis in tumors. In this article, a review of the literature concerning both pro-angiogenic and anti-angiogenic effects of resveratrol and the underlying mechanisms of its effects on angiogenesis is presented.
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PMID:Review. Pro- and anti-angiogenesis effects of resveratrol. 1743 89

The periods of ischemia and reperfusion represent different characteristics by lack of oxygen and reoxygenation. The aim of this experimental spinal cord injury model was to investigate whether resveratrol has protective effects during ischemia or reperfusion and the mechanism of the protection by using N-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase. Rabbits were divided into seven groups according to the time of administration of resveratrol or L-NAME (RI and RR, resveratrol during ischemia or reperfusion; IL and RL, L-NAME during ischemia or reperfusion; RILR, resveratrol during ischemia and L-NAME during reperfusion; LIRR, L-NAME during ischemia and resveratrol during reperfusion; control group). After neurologic evaluation at the twenty-fourth hour of reperfusion, lumbar spinal cords were removed for electron microscopic evaluation, immunohistochemical staining for apoptosis, and malondialdehyde (MDA) and myeloperoxidase (MPO) measurements. The RILR group had the best functional recovery, with a mean 3.6 Tarlov score (P < 0.05), and showed near normal electron microscopic findings (scores of 7.6 +/- 0.9 for the control group and 3.9 +/- 2.9 for the RILR group, P < 0.05). MPO and MDA levels were decreased in all groups compared with the control group, but only the decrement in the RILR group reached statistical significance. Immunohistochemical analysis showed that the groups including resveratrol and L-NAME together had the best staining for apoptosis. Resveratrol exhibits important protection by means of neurologic outcome, histopathologic analysis, and biochemical analysis, especially when used in during ischemia followed by L-NAME administration during reperfusion. Also, resveratrol protects against apoptosis, especially when combined with L-NAME.
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PMID:In which period of injury is resveratrol treatment effective: ischemia or reperfusion? 1839 12

This study is to explore whether the protective effect of resveratrol on ischemia-reperfusion injury is correlated with the structural and functional association between M3 receptor (M3 subtype of muscarinic acetylcholine receptor) and Cx43 (connexin 43 gap junction proteins). Immunoprecipitation, immunoblotting and immunofluorescence were applied to investigate whether resveratrol has an effect on structural and functional association between M3 and Cx43. The effect of resveratrol on electrocardiogram Lead II ex vivo in rats, SOD (superoxide dismutase) activity and MDA (malondialdehyde) content was also observed in order to evaluate the protective effect of resveratrol on ischemia-reperfusion injury. Resveratrol could restore the structural and functional association between M3 receptor and Cx43 gap junction proteins that was partially destroyed under ischemia-reperfusion injury. The phosphorylation and spatial distribution disturbances in Cx43 expression caused by ischemia-reperfusion injury were also restored. Also, the QRS duration, SOD activity and MDA content were restored. Resveratrol could restore the structural and functional association between M3 receptor and Cx43 gap junction proteins.
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PMID:[Resveratrol restored the structural and functional association between M3 receptor and connexin 43 gap junction proteins in ischemia-reperfusion injury of isolated rat heart]. 1752 Aug 2

Resveratrol, a natural polyphenolic compound, is found in a few edible materials and is well known for its phytoestrogenic and antioxidant properties. A growing body of in vivo and in vitro evidence indicates that resveratrol has protective effect on cerebral ischemic stroke. Here, we review the effect of resveratrol on cerebral ischemic stroke, and propose a possible mechanism. During acute phases after stroke, resveratrol preconditioning suppresses matrix metalloprotease-9 activity to ameliorate blood-brain barrier disruption, edema formation and neuronal cell death caused by ischemia and reperfusion. But during delayed phases after stroke, resveratrol preconditioning conduces to cerebral angiogenesis and brain regeneration through increasing matrix metalloprotease-9 activity and expression. Resveratrol's effect on matrix metalloprotease-9 is distinguishing in different phases because of temporal and spatial redistribution of matrix metalloprotease-9 within the cells of the neurovascular unit after cerebral ischemia. This paper also hypothesizes that resveratrol treatment after cerebral ischemia might be beneficial for cerebral angiogenesis and brain regeneration during delayed phases after stroke.
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PMID:New insights into mechanism for the effect of resveratrol preconditioning against cerebral ischemic stroke: Possible role of matrix metalloprotease-9. 1760 79

Moderate consumption of red wine is associated with a decreased incidence of cardiovascular diseases in populations with relatively high amount of fat in the diet. However, the mechanisms involved in this protective effect are not completely understood. Here we show that moderate consumption of red wine (equivalent to 2 glasses/day in humans) but not ethanol only, improves blood flow recovery by 32% after hindlimb ischemia in hypercholesterolemic ApoE-deficient mice. In ischemic tissues, red wine consumption reduces oxidative stress and increases capillary density by 46%. Endothelial progenitor cells (EPCs) have been shown to have an important role in postnatal neovascularization. We found that the number of EPCs is increased by 60% in ApoE mice exposed to red wine. Moreover, the migratory capacity of EPCs is significantly improved in red wine-drinking mice. The wine used in our study is a cabernet sauvignon from Languedoc-Roussillon, France, which contains a relatively high concentration (4-6 mg/L) of the polyphenolic antioxidant resveratrol. We demonstrate that resveratrol can rescue oxidized low-density lipoprotein (oxLDL)-induced impairment of in vitro angiogenic activities in human umbilical vein endothelial cells (HUVECs). Resveratrol exposure is also associated with increased activation of Akt/eNOS together with a restoration of nitric oxide production in HUVECs exposed to oxLDL. Our study suggests that moderate consumption of red wine improves ischemia-induced neovascularization in high-cholesterol conditions by increasing the number and the functional activities of EPCs and by restoring the Akt-eNOS-NO pathway.
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PMID:Moderate consumption of red wine (cabernet sauvignon) improves ischemia-induced neovascularization in ApoE-deficient mice: effect on endothelial progenitor cells and nitric oxide. 1764 Nov 50

Excessive oxidative stress has been implicated in the pathology and complications of diabetes, which leads to myocardial ischemia reperfusion injury. The present study was designed to examine whether resveratrol (trans-3,5,4'-trihydroxystilbene), a polyphenolic compound present in red wine has a direct cardioprotective effect on diabetic myocardium. Resveratrol (2.5 mg/kg body wt/day) and L-NAME (25 mg/kg body wt/day) were administered orally for 15 days to streptozotocin (65 mg/kg)-induced diabetic rats. Sprague Dawley rats were divided into 5 groups: (i) control, (ii) diabetic, (iii) diabetic+resveratrol, (iv) diabetic+resveratrol+L-NAME (nitric oxide synthase inhibitor), and (v) diabetic+L-NAME. In our present study resveratrol demonstrated significant reduction in glucose level in diabetic rats. After the treatment, the hearts were excised and subjected to 30 min of global ischemia followed by 2 h of reperfusion. Resveratrol-treated diabetic rats demonstrated significant reduction in glucose levels as compared to the nontreated diabetic animals, and improved left ventricular function throughout reperfusion compared to the diabetic or L-NAME-treated animals (dp/dt(max) 1457+/-51 vs 999+/-44 mm Hg/s at 120 min reperfusion). Cardioprotection from ischemic injury in resveratrol-treated diabetic rats showed decreased infarct size (42% vs 51%) and cardiomyocyte apoptosis (35% vs 40%) as compared with diabetic animals. Resveratrol produced significant induction of p-AKT, p-eNOS, Trx-1, HO-1, and VEGF in addition to increased activation of MnSOD activity in diabetic animals compared to nondiabetic animals. However treatment with L-NAME in resveratrol-treated and nontreated diabetic animals demonstrated significant downregulation of the above-noted protein expression profile and MnSOD activity. In the present study we found that the mechanism(s) responsible for the cardioprotective effect of resveratrol in the diabetic myocardium include upregulation of Trx-1, NO/HO-1, and VEGF in addition to increased MnSOD activity and reduced blood glucose level. Thus this study shows a novel mechanism of pharmacological preconditioning with resveratrol in the diabetic myocardium.
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PMID:Resveratrol alleviates cardiac dysfunction in streptozotocin-induced diabetes: Role of nitric oxide, thioredoxin, and heme oxygenase. 1766 36


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