Brain protection by resveratrol and fenofibrate against stroke requires peroxisome proliferator-activated receptor α in mice

Inoue, H.; Jiang, Xiao Fan; Katayama, Takahiro; Osada, Shiho; Umesono, Kazuhiko; Namura, Shobu

doi:10.1016/j.neulet.2003.09.001

Cited by 212 publications

(123 citation statements)

References 21 publications

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“…Other studies confirmed that resveratrol might reduce cerebral ischemic damage in different animal stroke models [136,137]. Gerbils injected with resveratrol intraperitoneally experienced decreased neuronal death in the hippocampus and had lower glial cell activation either during or shortly after common carotid artery (CCA) ligation and 24h later [138].…”

Section: B Experimental Studies In Animal Modelsmentioning

confidence: 79%

“…Resveratrol activates the PPAR-and PPAR-receptors which are recognized to have anti-inflammatory actions. This effect has been partially confirmed in PPAR-knockout mice where resveratrol does not reduce the infarct volume after MCA occlusion [136].…”

Section: B Experimental Studies In Animal Modelsmentioning

confidence: 88%

“…In rats, intravenous administration of different doses of resveratrol either 15 minutes before middle cerebral artery (MCA) occlusion or at its end provided a potent neuroprotective effect at the highest dosages [135]. The chronic treatment of rats with trans-resveratrol (daily intraperitoneal injection for 21days) after MCA occlusion prevented the rise of malondialdehyde (MDA) levels in the brain and decreased the volume of infarction as compared to controls [136]. In mice, a single dose of resveratrol given orally 1 hour before permanent MCA ligation does not protect against ischemic damage, while given daily for 3 days before ischemia it significantly reduces the infarct size [136].…”

Section: B Experimental Studies In Animal Modelsmentioning

confidence: 99%

“…The chronic treatment of rats with trans-resveratrol (daily intraperitoneal injection for 21days) after MCA occlusion prevented the rise of malondialdehyde (MDA) levels in the brain and decreased the volume of infarction as compared to controls [136]. In mice, a single dose of resveratrol given orally 1 hour before permanent MCA ligation does not protect against ischemic damage, while given daily for 3 days before ischemia it significantly reduces the infarct size [136]. Besides antioxidant activity, resveratrol may protect against brain damage via several mechanisms.…”

Section: B Experimental Studies In Animal Modelsmentioning

confidence: 99%

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Dietary Antioxidants as Potential Pharmacological Agents for Ischemic Stroke

Cherubini¹,

Ruggiero²,

Morand³

et al. 2008

CMC

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Acute ischemic stroke is a leading cause of death and severe disability in industrialised countries and also in many developing countries. An excessive amount of free radicals is generated during cerebral ischemia, which significantly contributes to brain damage. Therefore, an increasing interest has been devoted to the potential benefits of antioxidant compounds in ischemic stroke patients. In this review, we examined the most relevant observational studies concerning the relationship between dietary antioxidants and ischemic stroke as well as clinical trials investigating the effects of single or multiple antioxidant supplementation in the prevention or treatment of acute ischemic stroke. Furthermore, we reviewed the most promising antioxidant compounds, i.e. dehydroascorbic acid, alpha-tocotrienol, gamma-tocopherol, flavonoids, resveratrol and gingko biloba, tested in animal models of acute ischemic stroke. Finally, we carefully evaluated the reasons for the discrepancy between experimental and clinical studies, and provided recommendations to improve the translation of the results obtained in animal models to patients with acute ischemic stroke.

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Section: B Experimental Studies In Animal Modelsmentioning

confidence: 79%

Section: B Experimental Studies In Animal Modelsmentioning

confidence: 88%

Section: B Experimental Studies In Animal Modelsmentioning

confidence: 99%

Section: B Experimental Studies In Animal Modelsmentioning

confidence: 99%

See 2 more Smart Citations

Dietary Antioxidants as Potential Pharmacological Agents for Ischemic Stroke

Cherubini¹,

Ruggiero²,

Morand³

et al. 2008

CMC

View full text Add to dashboard Cite

show abstract

“…We have hypothesized that the suppression of cyclooxygenase-2 (COX-2) expression and the activation of peroxisome proliferator-activated receptors (PPARs) would be useful in evaluating the function of foodrelated components in lifestyle-related diseases. [1][2][3][4][5] COX, a key enzyme in prostaglandin biosynthesis, has two isoforms, COX-1 and -2. COX-1 is constitutively expressed in most cells, whilst COX-2 is primarily induced upon stimulation by such inflammatory stimuli as the endotoxin, lipopolysaccharide (LPS).…”

mentioning

confidence: 99%

Citronellol and Geraniol, Components of Rose Oil, Activate Peroxisome Proliferator-Activated Receptor α and γ and Suppress Cyclooxygenase-2 Expression

Katsukawa

Nakata

Koeji

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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Resveratrol and Its Metabolites Bind to PPARs

et al. 2014

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Resveratrol, a modulator of several signaling proteins, can exert off-target effects involving PPAR transcription factor. However, evidence for the direct interaction between this polyphenol and PPARs is lacking. Here, we addressed the hypothesis that resveratrol and its metabolites control aspects of PPAR transcriptional activity through direct interaction with PPARs. Bioaffinity chromatographic studies with the immobilized ligand-binding domains (LBDs) of PPARγ and PPARα and isothermal titration calorimetry (ITC) allowed the determination of the binding affinities of resveratrol, resveratrol 3-O-glucuronide, resveratrol 4-O-glucuronide and resveratrol 3-O-sulfate to both PPAR-LBDs. Interaction of resveratrol, resveratrol 3-O-glucuronide and resveratrol 4-O-glucuronide with PPARγ-LBD occurred with binding affinities of 1.4, 1.1 and 0.8 μM, respectively, while only resveratrol bound to the PPARα-LBD with a binding affinity of 2.7 μM. Subsequently, X-ray crystallographic studies were carried out to characterize resveratrol binding to the PPARγ-LBD at the molecular level. The electron density map from the crystal structure of the complex between PPARγ-LBD and resveratrol revealed the presence of one molecule of resveratrol bound into the LBD of PPARγ, with the ligand occupying a position close to that of other know PPARγ ligands. Transactivation assays were also performed in HepG2 cells and the results showed that resveratrol was not a PPAR agonist but, instead was able to displace rosiglitazone from PPARγ and Wy-14,643 from PPARα with IC50 values of 27.4 ± 1.8 μM and 31.7 ± 2.5 μM, respectively. We propose that resveratrol acts as a PPAR antagonist through its direct interaction with PPARγ and PPARα.

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Brain protection by resveratrol and fenofibrate against stroke requires peroxisome proliferator-activated receptor α in mice

Cited by 212 publications

References 21 publications

Dietary Antioxidants as Potential Pharmacological Agents for Ischemic Stroke

Dietary Antioxidants as Potential Pharmacological Agents for Ischemic Stroke

Citronellol and Geraniol, Components of Rose Oil, Activate Peroxisome Proliferator-Activated Receptor α and γ and Suppress Cyclooxygenase-2 Expression

Resveratrol and Its Metabolites Bind to PPARs

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