Sulforaphane reduces infarct volume following focal cerebral ischemia in rodents

Zhao, Jing; Kobori, Nobuhide; Aronowski, Jaroslaw; Dash, Pramod K.

doi:10.1016/j.neulet.2005.09.065

Cited by 221 publications

(163 citation statements)

References 28 publications

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“…Our current results reveal that HO1 is at least partially required for EC activity. A number of cerebral ischemia studies indicate that neuroprotective agents exert an effect through the Nrf2 detoxifying pathway (Satoh et al, 2006;Shih et al, 2005;Zhao et al, 2006). This pathway has also been suggested to be at least partially mediated through HO1 induction by electrophiles (Gong et al, 2002;Itoh et al, 2004;Loboda et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

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

Shah

Ahmad

et al. 2010

J Cereb Blood Flow Metab

203

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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Section: Discussionmentioning

confidence: 99%

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

Shah

Ahmad

et al. 2010

J Cereb Blood Flow Metab

203

125

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“…Sulforaphane shows neuroprotection in several rat models of acute brain injury, e.g., stroke (Zhao et al, 2006a) and head trauma (Zhao et al, 2005), in which evidence for mitochondrial PTP involvement exists (Kristian and Siesjo, 1998;Okonkwo and Povlishock, 1999). Rats fed a Figure 5 Neuroprotection by Nrf2-stimulated expression of cytoprotective genes.…”

Section: Protection Against Mitochondrial Oxidative Stressmentioning

confidence: 99%

Novel Mitochondrial Targets for Neuroprotection

Pérez-Pinzón

Stetler

Fiskum

2012

J Cereb Blood Flow Metab

124

108

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Mitochondrial dysfunction contributes to the pathophysiology of acute neurologic disorders and neurodegenerative diseases. Bioenergetic failure is the primary cause of acute neuronal necrosis, and involves excitotoxicity-associated mitochondrial Ca 2 + overload, resulting in opening of the inner membrane permeability transition pore and inhibition of oxidative phosphorylation. Mitochondrial energy metabolism is also very sensitive to inhibition by reactive O 2 and nitrogen species, which modify many mitochondrial proteins, lipids, and DNA/RNA, thus impairing energy transduction and exacerbating free radical production. Oxidative stress and Ca 2 + -activated calpain protease activities also promote apoptosis and other forms of programmed cell death, primarily through modification of proteins and lipids present at the outer membrane, causing release of proapoptotic mitochondrial proteins, which initiate caspase-dependent and caspase-independent forms of cell death. This review focuses on three classifications of mitochondrial targets for neuroprotection. The first is mitochondrial quality control, maintained by the dynamic processes of mitochondrial fission and fusion and autophagy of abnormal mitochondria. The second includes targets amenable to ischemic preconditioning, e.g., electron transport chain components, ion channels, uncoupling proteins, and mitochondrial biogenesis. The third includes mitochondrial proteins and other molecules that defend against oxidative stress. Each class of targets exhibits excellent potential for translation to clinical neuroprotection.

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“…In addition to affecting membrane biophysical properties, PUFAs in the form of phospholipids in neuronal membranes can also directly participate in signaling cascades to promote synaptic plasticity, neuronal function and neuroprotection. 35 Seabuckthorn seed oil is rich with omega-3: omega-6 (1:1) and also revealed that it has the cerebral cardiovascular functions by coordination of neurons. 65…”

Section: Fatty Acidsmentioning

confidence: 99%

Phytochemicals Having Neuroprotective Properties from Dietary Sources and Medicinal Herbs

Kumar¹,

Anilakumar²,

Naveen³

2015

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Many neuropsychiatric and neurodegenerative disorders, such as Alzheimer's disease, anxiety, cerebrovascular impairment, depression, seizures, Parkinson's disease, etc. are predominantly appearing in the current era due to the stress full lifestyle. Treatment of these disorders with prolonged administration of synthetic drugs will lead to severe side effects. In the recent years, scientists have focused the attention of research towards phytochemicals to cure neurological disorders. Nootropic herb refers to the medicinal role of various plants/parts for their neuroprotective properties by the active phytochemicals including alkaloids, steroids, terpenoids, saponins, phenolics, flavonoids, etc. Phytocompounds from medicinal plants play a major part in maintaining the brain's chemical balance by acting upon the function of receptors for the major inhibitory neurotransmitters. Medicinal plants viz. Valeriana officinalis, Nardostachys jatamansi, Withania somnifera, Bacopa monniera, Ginkgo biloba and Panax ginseng have been used widely in a variety of traditional systems of therapy because of their adaptogenic, psychotropic and neuroprotective properties. This review highlights the importance of phytochemicals on neuroprotective function and other related disorders, in particular their mechanism of action and therapeutic potential.

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Sulforaphane reduces infarct volume following focal cerebral ischemia in rodents

Cited by 221 publications

References 28 publications

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

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

Novel Mitochondrial Targets for Neuroprotection

Phytochemicals Having Neuroprotective Properties from Dietary Sources and Medicinal Herbs

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