NDLI: Neurological and Histological Consequences Induced by In Vivo Cerebral Oxidative Stress: Evidence for Beneficial Effects of SRT1720, a Sirtuin 1 Activator, and Sirtuin 1-Mediated Neuroprotective Effects of Poly(ADP-ribose) Polymerase Inhibition

Content Provider	PubMed Central
Author	Gueguen, Cindy Palmier, Bruno Michel, Plotkine Catherine, Marchand-leroux Besson, Valérie C.
Editor	Padmanabhan, Jaya
Copyright Year	2014
Abstract	Poly(ADP-ribose)polymerase and sirtuin 1 are both NAD+-dependent enzymes. In vitro oxidative stress activates poly(ADP-ribose)polymerase, decreases NAD+ level, sirtuin 1 activity and finally leads to cell death. Poly(ADP-ribose)polymerase hyperactivation contributes to cell death. In addition, poly(ADP-ribose)polymerase inhibition restores NAD+ level and sirtuin 1 activity in vitro. In vitro sirtuin 1 induction protects neurons from cell loss induced by oxidative stress. In this context, the role of sirtuin 1 and its involvement in beneficial effects of poly(ADP-ribose)polymerase inhibition were evaluated in vivo in a model of cerebral oxidative stress induced by intrastriatal infusion of malonate in rat. Malonate promoted a NAD+ decrease that was not prevented by 3-aminobenzamide, a poly(ADP-ribose)polymerase inhibitor, at 4 and 24 hours. However, 3-aminobenzamide increased nuclear SIRT1 activity/expression ratio after oxidative stress. Malonate induced a neurological deficit associated with a striatal lesion. Both were reduced by 3-aminobenzamide and SRT1720, a sirtuin 1 activator, showing beneficial effects of poly(ADP-ribose)polymerase inhibition and sirtuin 1 activation on oxidative stress consequences. EX527, a sirtuin 1 inhibitor, given alone, modified neither the score nor the lesion, suggesting that endogenous sirtuin 1 was not activated during cerebral oxidative stress. However, its association with 3-aminobenzamide suppressed the neurological improvement and the lesion reduction induced by 3-aminobenzamide. The association of 3-aminobenzamide with SRT1720, the sirtuin 1 activator, did not lead to a better protection than 3-aminobenzamide alone. The present data represent the first demonstration that the sirtuin 1 activator SRT1720 is neuroprotective during in vivo cerebral oxidative stress. Furthermore sirtuin 1 activation is involved in the beneficial effects of poly(ADP-ribose)polymerase inhibition after in vivo cerebral oxidative stress.
Related Links	http://dx.doi.org/10.1371/journal.pone.0087367
Starting Page	87367
File Format	PDF
ISSN	19326203
e-ISSN	19326203
Journal	PLoS ONE
Issue Number	2
Volume Number	9
Language	English
Publisher	Public Library of Science
Publisher Date	2014-02-01
Access Restriction	Open
Rights Holder	Public Library of Science
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Agricultural and Biological Sciences(all) Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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Correction: Neurological and Histological Consequences Induced by In Vivo Cerebral Oxidative Stress: Evidence for Beneficial Effects of SRT1720, a Sirtuin 1 Activator, and Sirtuin 1-Mediated Neuroprotective Effects of Poly(ADP-ribose) Polymerase Inhibition

Correction: Neurological and Histological Consequences Induced by In Vivo Cerebral Oxidative Stress: Evidence for Beneficial Effects of SRT1720, a Sirtuin 1 Activator, and Sirtuin 1-Mediated Neuroprotective Effects of Poly(ADP-ribose) Polymerase Inhibition

Poly(ADP-ribose) polymerase-1 protects neurons against apoptosis induced by oxidative stress

Poly(ADP-ribose) polymerase inhibition improves endothelin-1-induced endothelial dysfunction in rat thoracic aorta

Modulation of urokinase plasminogen activator system by poly(ADP-ribose)polymerase-1 inhibition

Dynamic Interplay between Cockayne Syndrome Protein B and Poly(ADP-Ribose) Polymerase 1 during Oxidative DNA Damage Repair

Poly(ADP-ribose) polymerase-1-induced NAD+ depletion promotes nuclear factor-κB transcriptional activity by preventing p65 de-acetylation

Crosstalk between poly(ADP-ribose) polymerase and sirtuin enzymes.

Poly(ADP-ribose) polymerase-1-induced NAD(+) depletion promotes nuclear factor-κB transcriptional activity by preventing p65 de-acetylation.

Neurological and Histological Consequences Induced by In Vivo Cerebral Oxidative Stress: Evidence for Beneficial Effects of SRT1720, a Sirtuin 1 Activator, and Sirtuin 1-Mediated Neuroprotective Effects of Poly(ADP-ribose) Polymerase Inhibition

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Correction: Neurological and Histological Consequences Induced by In Vivo Cerebral Oxidative Stress: Evidence for Beneficial Effects of SRT1720, a Sirtuin 1 Activator, and Sirtuin 1-Mediated Neuroprotective Effects of Poly(ADP-ribose) Polymerase Inhibition

Correction: Neurological and Histological Consequences Induced by In Vivo Cerebral Oxidative Stress: Evidence for Beneficial Effects of SRT1720, a Sirtuin 1 Activator, and Sirtuin 1-Mediated Neuroprotective Effects of Poly(ADP-ribose) Polymerase Inhibition

Poly(ADP-ribose) polymerase-1 protects neurons against apoptosis induced by oxidative stress

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Poly(ADP-ribose) polymerase-1-induced NAD+ depletion promotes nuclear factor-κB transcriptional activity by preventing p65 de-acetylation

Crosstalk between poly(ADP-ribose) polymerase and sirtuin enzymes.

Poly(ADP-ribose) polymerase-1-induced NAD(+) depletion promotes nuclear factor-κB transcriptional activity by preventing p65 de-acetylation.

Neurological and Histological Consequences Induced by In Vivo Cerebral Oxidative Stress: Evidence for Beneficial Effects of SRT1720, a Sirtuin 1 Activator, and Sirtuin 1-Mediated Neuroprotective Effects of Poly(ADP-ribose) Polymerase Inhibition