Polyphenols in Cerebral Ischemia: Novel Targets for Neuroprotection

Simonyi, Ágnes; Wang, Qun; Miller, Rebecca L.; Yusof, Mozow; Shelat, Phullara B.; Sun, Albert Y.; Sun, Grace Y.

doi:10.1385/mn:31:1-3:135

Cited by 145 publications

(89 citation statements)

References 85 publications

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“…The brain is quite susceptible to oxidative stress due to its environment with non-heme iron, which is involved catalytically in the production of free radicals (26). The close relationship between oxidative stress and cerebral ischemia has generated considerable interest in the development of antioxidant therapies to combat ischemia-induced damage (27,28). Our results showed that the administration of KRG ameliorated brain injury subsequent to MCAO/R in rats.…”

Section: Discussionmentioning

confidence: 57%

Korean red ginseng protects against neuronal damage induced by transient focal ischemia in rats

Ban

Kang

Lee

et al. 2012

Experimental and Therapeutic Medicine

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Abstract. In the present study, we investigated the neuroprotective effect of Korean red ginseng (KRG) following focal brain ischemia/reperfusion injury, in relation to its antioxidant activities. The middle cerebral artery occlusion/reperfusion (MCAO/R) model in rats was employed. The KRG extract (100 mg/kg, perorally) was administered once daily for 7 days following MCAO/R. The elevated levels of lipid peroxidation in the MCAO/R group were attenuated significantly in the KRG-administered group. The significantly depleted activity of the antioxidant enzymes glutathione peroxidase, superoxide dismutase and catalase was prevented in the KRG-administered group. In the neurobehavioral evaluation expressed as the modified neurological severity score and corner-turn test, the daily intake of KRG showed consistent and significant improvement in the neurological deficits for 7 days following MCAO/R injury. These results indicate that KRG has a neuroprotective effect against ischemia/reperfusion brain injury by reducing the level of lipid peroxidation and increasing the endogenous antioxidant enzymatic activity.

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Section: Discussionmentioning

confidence: 57%

Korean red ginseng protects against neuronal damage induced by transient focal ischemia in rats

Ban

Kang

Lee

et al. 2012

Experimental and Therapeutic Medicine

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“…Numerous epidemiologic studies have revealed a strong inverse correlation between ischemic heart disease and consumption of red wine and certain fruits and vegetables that contain high levels of flavonoids and other polyphenols (Simonyi et al, 2005). Flavanols (e.g., epicatechin (EC) and catechin) and their monomers/oligomers/polymers, known as procyanidins, compose a major category of secondary polyphenolic plant metabolites.…”

Section: Introductionmentioning

confidence: 99%

The Flavanol (−)-Epicatechin Prevents Stroke Damage through the Nrf2/HO1 Pathway

Shah

Ahmad

et al. 2010

J Cereb Blood Flow Metab

208

125

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Epidemiologic studies have shown that foods rich in polyphenols, such as flavanols, can lower the risk of ischemic heart disease; however, the mechanism of protection has not been clearly established. In this study, we investigated whether epicatechin (EC), a flavanol in cocoa and tea, is protective against brain ischemic damage in mice. Wild-type mice pretreated orally with 5, 15, or 30 mg/kg EC before middle cerebral artery occlusion (MCAO) had significantly smaller brain infarcts and decreased neurologic deficit scores (NDS) than did the vehicle-treated group. Mice that were posttreated with 30 mg/kg of EC at 3.5 hours after MCAO also had significantly smaller brain infarcts and decreased NDS. Similarly, WT mice pretreated with 30 mg/kg of EC and subjected to N-methyl-D-aspartate (NMDA)-induced excitotoxicity had significantly smaller lesion volumes. Cell viability assays with neuronal cultures further confirmed that EC could protect neurons against oxidative insults. Interestingly, the EC-associated neuroprotection was mostly abolished in mice lacking the enzyme heme oxygenase 1 (HO1) or the transcriptional factor Nrf2, and in neurons derived from these knockout mice. These results suggest that EC exerts part of its beneficial effect through activation of Nrf2 and an increase in the neuroprotective HO1 enzyme.

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“…However, data on the bioavailability of these plant extracts are largely lacking (Loew and Kaszkin, 2002;Simonyi et al, 2005;Williamson and Manach, 2005). In our previous work, we investigated the bioavailability of two plant polyphenolic compounds, resveratrol and curcumin, extracted from grapes and turmeric, respectively (Wang et al, 2002;Wang et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Bioavailability of apocynin through its conversion to glycoconjugate but not to diapocynin

et al. 2008

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Apocynin (4-hydroxy-3-methoxyacetophenone) is a major active ingredient from the rhizomes of Picrorhiza kurroa, a botanical plant used as an herbal medicine for treatment of a number of inflammatory diseases. Recently, apocynin is regarded as a specific inhibitor for NADPH oxidase in cell and animal models. In vitro studies indicated conversion of apocynin to diapocynin in the presence of peroxidases, e.g., myloperoxidase, posing the possibility that diapocynin also contributes to the anti-oxidative action of apocynin. The objectives of this study are to examine the bioavailability of apocynin to plasma, liver and brain tissue after intraperitoneal (i.p.) injection, and to examine whether apocynin is converted to diapocynin in vivo. Diapocynin was chemically synthetized and characterized by NMR and IR. Apocynin (5 mg/kg body wt) was injected i.p. to adult male Sprague-Dawley rats and plasma, liver and brain were collected at different times (30 min, 1 h and 2 h) after injection. Samples were treated with β-glucuronidase to hydrolyze the glycosyl linkage and analyzed by HPLC/MS. At 30 min and 1 h after injection, approximately 50% of apocynin was converted to its glycosyl derivative and was distributed in plasma, liver and brain. No diapocynin was detected in any samples. These results indicate rapid glycosylation of apocynin and its transport to blood and other organs but no apparent conversion to diapocynin in vivo.

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Polyphenols in Cerebral Ischemia: Novel Targets for Neuroprotection

Cited by 145 publications

References 85 publications

Korean red ginseng protects against neuronal damage induced by transient focal ischemia in rats

Korean red ginseng protects against neuronal damage induced by transient focal ischemia in rats

The Flavanol (−)-Epicatechin Prevents Stroke Damage through the Nrf2/HO1 Pathway

Bioavailability of apocynin through its conversion to glycoconjugate but not to diapocynin

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