Non-steroidal anti-inflammatory agents, tolmetin and sulindac attenuate quinolinic acid (QA)-induced oxidative stress in primary hippocampal neurons and reduce QA-induced spatial reference memory deficits in male Wistar rats

Dairam, Amichand; Müller, Adrienne; Daya, Santy

doi:10.1016/j.lfs.2007.01.006

Cited by 12 publications

(10 citation statements)

References 51 publications

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“…Sulindac, administered topically or in the drinking water, protected the skin of SKH-1 hairless mice in response to UV light (42). Sulindac has also been reported to decrease age related defects in learning and memory in rats (43) and was found to prevent the depletion of GSH in the hippocampus under conditions of quinolinic acid induced oxidative stress (44).…”

Section: Discussionmentioning

confidence: 99%

Sulindac confers high level ischemic protection to the heart through late preconditioning mechanisms

Moench

Prentice

Rickaway³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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We have recently shown that sulindac, an anti-inflammatory drug, enhances the killing of cancer cells, but not normal cells, under conditions of oxidative stress, by mechanisms unrelated to its cyclooxygenase (COX) inhibition. To further study the protective effect of sulindac on cells exposed to oxidative stress, we have investigated the effect of sulindac on rat cardiac myocytes subjected to hypoxia/reoxygenation, as well as in a Langendorff model of myocardial ischemia. Low levels of sulindac could protect cardiac myocytes against cell death due to hypoxia/reoxygenation. In the Langendorff model sulindac provided significant protection against cell death, when the drug was fed to the animals before the removal of the heart for the Langendorff procedure. The results indicate that the primary protective effect of sulindac in these experiments does not involve its role as a COX inhibitor. Numerous signaling pathways have been implicated in myocardial protective mechanisms, many of which involve fluctuations in reactive oxygen species (ROS) levels. The results suggest that low levels of sulindac can induce a preconditioning response, triggered by ROS, to protect cardiac tissues against oxidative damage. Blocking of preconditioning pathways by administration of the PKC blocker chelerythrine abrogated the ischemic protection afforded by sulindac. Secondly, after feeding of sulindac, two end-effectors of preconditioning, inducible nitric oxide synthase and heat shock protein 27, were found to be markedly induced in the heart, dependent on PKC. These results suggest that sulindac may have therapeutic potential as a preconditioning agent.cardioprotection ͉ myocardial ischemia

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Section: Discussionmentioning

confidence: 99%

Sulindac confers high level ischemic protection to the heart through late preconditioning mechanisms

Moench

Prentice

Rickaway³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…If an analogous fibril maturation mechanism operates in vivo, the protofibril stage could be an important therapeutic focus. In vivo experiments using transgenic mice overexpress Aβ protein precursor and develop characteristic Aβ deposits within the brain parenchyma (Poeggeler et al, 2001) and demonstrating the same type of oxidative damage that is found in AD (Dairam et al, 2007;Pratico et al, 2001). Life Sciences 83 (2008) [96][97][98][99][100][101][102] A constant feature in AD brain is selective neuronal loss, accompanied by dysfunction of several neurotransmitter systems, such as cholinergic, serotoninergic and noradrenergic systems (Bell and Claudio Cuello 2006;Lehericy et al, 1993;Szot et al, 2000).…”

Section: Introductionmentioning

confidence: 94%

Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism

et al. 2008

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“…As it has been demonstrated in the literature, the neural structures especially the hippocampal area has a specific vulnerability to ischemia-reperfusion injury process 8,14,15 .…”

Section: Discussionmentioning

confidence: 82%

“…Numerous studies revealed that ROS are directly involved in oxidative damage of cellular macromolecules such as proteins, lipids, and nucleic acids in tissues 5,7,17,19 . Neural structures especially hippocampus are the most vulnerable organs which are affected by ischemic-reperfusion injury 8,14 . In our study, we used MDA, MPO and GSH to demonstrate the level of I/R injury and the possible protective effect of Sulindac on the oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

“…Beside the its primary mechanism such as inhibition of prostaglandine synthesis by inhibiting cyclo-oxygenase constitutes, also the free radical scavenging activity of it for all ROS and reactive nitrogen species may strongly contribute to its anti-inflammatory activity 7 . In addition to all these, a growing body of evidence shows that Sulindac has remarkable neuroprotective effects via reduction of protein oxidation in neuroischemic diseases 8,9 .…”

Section: Introductionmentioning

confidence: 99%

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The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats

Çoşar¹,

Kaner

Şahin

et al. 2014

Acta Cir. Bras.

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PURPOSE:To investigate the neuroprotective effects of Sulindac on the hippocampal complex after global cerebral ischemia/reperfusion (I/R) injury in rats. METHODS:Thirty one Sprague-Dawley rats were used, distributed into group I (sham) n:7 were used as control. For group II (n:8), III (n:8) and IV (n:8) rats, cerebral ischemia was performed via the occlusion of bilateral internal carotid artery for 45 minutes and continued with reperfusion process. 0.3 mL/kg/h 0.9 % sodium chloride was infused intraperitoneally to the Group II rats before ischemia, 5µg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group III rats before ischemia and 5µg/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group IV rats after ischemia and before reperfusion process. The levels of MDA, GSH and MPO activity were measured in the left hippocampus tissue. The hippocampal tissue of all group members were taken for histopathological study.

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Non-steroidal anti-inflammatory agents, tolmetin and sulindac attenuate quinolinic acid (QA)-induced oxidative stress in primary hippocampal neurons and reduce QA-induced spatial reference memory deficits in male Wistar rats

Cited by 12 publications

References 51 publications

Sulindac confers high level ischemic protection to the heart through late preconditioning mechanisms

Sulindac confers high level ischemic protection to the heart through late preconditioning mechanisms

Melatonin prevents amyloid protofibrillar induced oxidative imbalance and biogenic amine catabolism

The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats

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