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Nutraceutical antioxidants as novel neuroprotective agents.

Kelsey NA, Wilkins HM, Linseman DA - Molecules (2010)

Bottom Line: These natural antioxidants fall into several distinct groups based on their chemical structures: (1) flavonoid polyphenols like epigallocatechin 3-gallate (EGCG) from green tea and quercetin from apples; (2) non-flavonoid polyphenols such as curcumin from tumeric and resveratrol from grapes; (3) phenolic acids or phenolic diterpenes such as rosmarinic acid or carnosic acid, respectively, both from rosemary; and (4) organosulfur compounds including the isothiocyanate, L-sulforaphane, from broccoli and the thiosulfonate allicin, from garlic.All of these compounds are generally considered to be antioxidants.Alternative mechanisms of action have also been suggested for the neuroprotective effects of these compounds such as modulation of signal transduction cascades or effects on gene expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences and Eleanor Roosevelt Institute, University of Denver, Denver, Colorado 80208, USA. nkelsey@du.edu

ABSTRACT
A variety of antioxidant compounds derived from natural products (nutraceuticals) have demonstrated neuroprotective activity in either in vitro or in vivo models of neuronal cell death or neurodegeneration, respectively. These natural antioxidants fall into several distinct groups based on their chemical structures: (1) flavonoid polyphenols like epigallocatechin 3-gallate (EGCG) from green tea and quercetin from apples; (2) non-flavonoid polyphenols such as curcumin from tumeric and resveratrol from grapes; (3) phenolic acids or phenolic diterpenes such as rosmarinic acid or carnosic acid, respectively, both from rosemary; and (4) organosulfur compounds including the isothiocyanate, L-sulforaphane, from broccoli and the thiosulfonate allicin, from garlic. All of these compounds are generally considered to be antioxidants. They may be classified this way either because they directly scavenge free radicals or they indirectly increase endogenous cellular antioxidant defenses, for example, via activation of the nuclear factor erythroid-derived 2-related factor 2 (Nrf2) transcription factor pathway. Alternative mechanisms of action have also been suggested for the neuroprotective effects of these compounds such as modulation of signal transduction cascades or effects on gene expression. Here, we review the literature pertaining to these various classes of nutraceutical antioxidants and discuss their potential therapeutic value in neurodegenerative diseases.

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Related in: MedlinePlus

EGCG protects neurons from oxidative stress. Representative images of CGNs incubated for 24 hrs with the Bcl-2 inhibitor HA14-1 (15 M), HA14-1 + EGCG (25 M), or no treatment (Control). Immunocytochemistry was performed for β-tubulin (green) and active caspase-3 (red). Nuclei are stained with DAPI, blue. Scale bar; 10 microns.
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Figure 2: EGCG protects neurons from oxidative stress. Representative images of CGNs incubated for 24 hrs with the Bcl-2 inhibitor HA14-1 (15 M), HA14-1 + EGCG (25 M), or no treatment (Control). Immunocytochemistry was performed for β-tubulin (green) and active caspase-3 (red). Nuclei are stained with DAPI, blue. Scale bar; 10 microns.

Mentions: EGCG (Figure 1A) is a flavonoid polyphenol and the main antioxidant compound found in green tea. EGCG displays neuroprotective effects in a variety of in vitro paradigms. Our own work has shown that EGCG selectively protects cultured rat cerebellar granule neurons (CGNs) from oxidative stress [28]. Figure 2 shows the dramatic effects EGCG has against oxidative stress in the CGN model. CGNs incubated with the Bcl-2 inhibitor, HA14-1 (ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate), undergo mitochondrial oxidative stress and intrinsic apoptosis [29,30]. Co-treatment with EGCG significantly preserves the microtubule network and prevents the apoptotic nuclear morphology of CGNs exposed to HA14-1 (Figure 2).


Nutraceutical antioxidants as novel neuroprotective agents.

Kelsey NA, Wilkins HM, Linseman DA - Molecules (2010)

EGCG protects neurons from oxidative stress. Representative images of CGNs incubated for 24 hrs with the Bcl-2 inhibitor HA14-1 (15 M), HA14-1 + EGCG (25 M), or no treatment (Control). Immunocytochemistry was performed for β-tubulin (green) and active caspase-3 (red). Nuclei are stained with DAPI, blue. Scale bar; 10 microns.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4697862&req=5

Figure 2: EGCG protects neurons from oxidative stress. Representative images of CGNs incubated for 24 hrs with the Bcl-2 inhibitor HA14-1 (15 M), HA14-1 + EGCG (25 M), or no treatment (Control). Immunocytochemistry was performed for β-tubulin (green) and active caspase-3 (red). Nuclei are stained with DAPI, blue. Scale bar; 10 microns.
Mentions: EGCG (Figure 1A) is a flavonoid polyphenol and the main antioxidant compound found in green tea. EGCG displays neuroprotective effects in a variety of in vitro paradigms. Our own work has shown that EGCG selectively protects cultured rat cerebellar granule neurons (CGNs) from oxidative stress [28]. Figure 2 shows the dramatic effects EGCG has against oxidative stress in the CGN model. CGNs incubated with the Bcl-2 inhibitor, HA14-1 (ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate), undergo mitochondrial oxidative stress and intrinsic apoptosis [29,30]. Co-treatment with EGCG significantly preserves the microtubule network and prevents the apoptotic nuclear morphology of CGNs exposed to HA14-1 (Figure 2).

Bottom Line: These natural antioxidants fall into several distinct groups based on their chemical structures: (1) flavonoid polyphenols like epigallocatechin 3-gallate (EGCG) from green tea and quercetin from apples; (2) non-flavonoid polyphenols such as curcumin from tumeric and resveratrol from grapes; (3) phenolic acids or phenolic diterpenes such as rosmarinic acid or carnosic acid, respectively, both from rosemary; and (4) organosulfur compounds including the isothiocyanate, L-sulforaphane, from broccoli and the thiosulfonate allicin, from garlic.All of these compounds are generally considered to be antioxidants.Alternative mechanisms of action have also been suggested for the neuroprotective effects of these compounds such as modulation of signal transduction cascades or effects on gene expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences and Eleanor Roosevelt Institute, University of Denver, Denver, Colorado 80208, USA. nkelsey@du.edu

ABSTRACT
A variety of antioxidant compounds derived from natural products (nutraceuticals) have demonstrated neuroprotective activity in either in vitro or in vivo models of neuronal cell death or neurodegeneration, respectively. These natural antioxidants fall into several distinct groups based on their chemical structures: (1) flavonoid polyphenols like epigallocatechin 3-gallate (EGCG) from green tea and quercetin from apples; (2) non-flavonoid polyphenols such as curcumin from tumeric and resveratrol from grapes; (3) phenolic acids or phenolic diterpenes such as rosmarinic acid or carnosic acid, respectively, both from rosemary; and (4) organosulfur compounds including the isothiocyanate, L-sulforaphane, from broccoli and the thiosulfonate allicin, from garlic. All of these compounds are generally considered to be antioxidants. They may be classified this way either because they directly scavenge free radicals or they indirectly increase endogenous cellular antioxidant defenses, for example, via activation of the nuclear factor erythroid-derived 2-related factor 2 (Nrf2) transcription factor pathway. Alternative mechanisms of action have also been suggested for the neuroprotective effects of these compounds such as modulation of signal transduction cascades or effects on gene expression. Here, we review the literature pertaining to these various classes of nutraceutical antioxidants and discuss their potential therapeutic value in neurodegenerative diseases.

Show MeSH
Related in: MedlinePlus