Apoptosis and the Nervous System

Sastry, P. S. N.; Rao, K. S.

doi:10.1046/j.1471-4159.2000.0740001.x

Cited by 409 publications

(242 citation statements)

References 205 publications

(312 reference statements)

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“…Recently, we have found that administration of the cyclooxygenase-2 inhibitor nimesulide at a dose proven to confer protection in the present study (6 mg/kg), is able to reduce hippocampal oxidative damage following excitotoxic brain injury (Candelario-Jalil et al, 2000), which is a key pathological event of cerebral ischemia. This latter observation is particularly relevant in view of evidence showing that oxidative stress is implicated in the development and progression of apoptotic cell death in the central nervous system (Sastry and Rao, 2000) and that activation of cyclooxygenase-2 is required for execution of oxidative neuronal death (Lee et al, 2001). Further experiments are needed to clarify the effects of selective inhibition of cyclooxygenase-2 on markers of oxidative stress in the ischemic brain and its relation to neuronal death after ischemia.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective efficacy of nimesulide against hippocampal neuronal damage following transient forebrain ischemia

Candelario‐Jalil

Alvarez

González-Falcón

et al. 2002

European Journal of Pharmacology

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Cyclooxygenase-2 is involved in the inflammatory component of the ischemic cascade, playing an important role in the delayed progression of the brain damage. The present study evaluated the pharmacological effects of the selective cyclooxygenase-2 inhibitor nimesulide on delayed neuronal death of hippocampal CA1 neurons following transient global cerebral ischemia in gerbils.Administration of therapeutically relevant doses of nimesulide (3, 6 and 12 mg/kg; i.p.) 30 minutes before ischemia and at 6, 12, 24, 48 and 72 h after ischemia significantly (P<0.01) reduced hippocampal neuronal damage. Treatment with a single dose of nimesulide given 30 min before ischemia also resulted in a significant increase in the number of healthy neurons in the hippocampal CA1 sector 7 days after ischemia. Of interest is the finding that nimesulide rescued CA1 pyramidal neurons from ischemic death even when treatment was delayed until 24 h after ischemia (34 ± 9 % protection). Neuroprotective effect of nimesulide is still evident 30 days after the ischemic episode, providing the first experimental evidence that cyclooxygenase-2 inhibitors confer a long lasting neuroprotection. Oral administration of nimesulide was also able to significantly reduce brain damage, suggesting that protective effects are independent of the route of administration. The present study confirms the ability of cyclooxygenase-2 inhibitors to reduce brain damage induced by cerebral ischemia and indicates that nimesulide can provide protection when administered for up to 24 h post-ischemia.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective efficacy of nimesulide against hippocampal neuronal damage following transient forebrain ischemia

Candelario‐Jalil

Alvarez

González-Falcón

et al. 2002

European Journal of Pharmacology

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“…To date, a number of neuronal cell culture models that were treated with different apoptotic agents such as protein S100B, cytokines, 3,4-methyl-enedioxy-methamphetamine or NO donors, show that the cells undergo apoptosis with the formation of NO (31). NO can release cytochrome C from mitochondria (32) and the apoptotic mechanism includes caspase-3 activation following down-regulation of Bcl-2 and up-regulation of Bax protein levels (33).…”

Section: Discussionmentioning

confidence: 99%

Plasma nitrite/nitrate concentrations in patients with schizophrenia

Djordjević¹,

Stojanović²,

Stankovic-Ferlez³

et al. 2010

Clinical Chemistry and Laboratory Medicine

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Background: Nitric oxide (NO) is known to be a signaling molecule with many physiogical functions including apoptotic process regulation. Since apoptosis may contribute to the pathophysiology of schizophrenia, this study was undertaken to determine the plasma concentrations of NO in schizophrenics. Methods: Nitrite/nitrate (NO 2 -/NO 3 -) concentrations were measured in plasma from 40 patients with schizophrenia, and 36 age-and gender-matched healthy persons using a colorimetric test. Results: Plasma NO 2 -/NO 3 -concentrations were significantly higher in patients with schizophrenia (102.8"34.7

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“…Altered lipid metabolism is believed to contribute to cerebral ischemic injury. [21][22][23][24][25][26][27][28][29][30][31][32] Lipidomics holds the promise of characterizing complex mixtures of lipids, identifying previously unknown changes in lipid metabolism, and opening new opportunities for drug development. 33 …”

Section: Focal Cerebral Ischemia (Stroke)mentioning

confidence: 99%

Lipids and lipidomics in brain injury and diseases

Adibhatla

Hatcher

Dempsey

2006

AAPS J

147

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Lipidomics is systems-level analysis and characterization of lipids and their interacting moieties. The amount of information in the genomic and proteomic fi elds is greater than that in the lipidomics fi eld, because of the complex nature of lipids and the limitations of tools for analysis. The main innovation during recent years that has spurred advances in lipid analysis has been the development of new mass spectroscopic techniques, particularly the " soft ionization " techniques electrospray ionization and matrix-assisted laser desorption/ionization. Lipid metabolism may be of particular importance for the central nervous system, as it has a high concentration of lipids. The crucial role of lipids in cell signaling and tissue physiology is demonstrated by the many neurological disorders, including bipolar disorders and schizophrenia, and neurodegenerative diseases such as Alzheimer ' s, Parkinson ' s, and Niemann-Pick diseases, that involve deregulated lipid metabolism. Altered lipid metabolism is also believed to contribute to cerebral ischemic (stroke) injury. Lipidomics will provide a molecular signature to a certain pathway or a disease condition. Lipidomic analyses (characterizing complex mixtures of lipids and identifying previously unknown changes in lipid metabolism) together with RNA silencing, using small interfering RNA (siRNA), may provide powerful tools to elucidate the specifi c roles of lipid intermediates in cell signaling and open new opportunities for drug development.K e yw o r ds: Acrolein , arachidonic acid , cerebral ischemia , cytidine-5 ′ -diphosphocholine , CDP-choline , citicoline , docosahexaenoic acid , 4-hydroxynonenal , lipidomics , lipid peroxidation , MALDI-TOF , ESI-MS-MS , neuroprotectin D1 , 10,17S-docosatriene , phospholipases , phospholipids , RNA silencing , small interfering RNA , siRNA , reactive oxygen species , stroke INTRODUCTIONPhospholipids are important components of all mammalian cells and have a variety of biological functions: (1) they form lipid bilayers that provide structural integrity necessary for protein function, (2) they function as an energy reservoir (eg, triglycerides), and (3) they serve as precursors for various second messengers such as arachidonic acid, docosahexaenoic acid, ceramide, 1,2-diacylglycerol, phosphatidic acid, and lyso-phosphatidic acid. A deeper knowledge of the complexity of phospholipid metabolism will elevate our understanding of the role of lipids in maintaining normal cell physiology and how alterations in lipid metabolism contribute to various disease states. DEFINING A LIPIDLipids comprise an enormous number of chemically distinct molecules arising from combinations of fatty acids with various backbone structures. Indeed, it is diffi cult to defi ne what lipids are. Defi ning lipids as a class of biological molecules that share a high degree of solubility in organic solvents is considered at once too broad and too narrow, encompassing structurally and functionally unrelated molecules and excluding lipids, such as ganglioside...

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Apoptosis and the Nervous System

Cited by 409 publications

References 205 publications

Neuroprotective efficacy of nimesulide against hippocampal neuronal damage following transient forebrain ischemia

Neuroprotective efficacy of nimesulide against hippocampal neuronal damage following transient forebrain ischemia

Plasma nitrite/nitrate concentrations in patients with schizophrenia

Lipids and lipidomics in brain injury and diseases

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