Neuroprotective effects of arachidonic acid against oxidative stress on rat hippocampal slices

Wang, Zejian; Liang, Cui-Ling; Li, Guang-Mei; Yu, Cai-Yi; Yin, Ming

doi:10.1016/j.cbi.2006.08.005

Cited by 110 publications

(63 citation statements)

References 41 publications

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“…In the MCAo + hMSC group, saturated FFAs, which have cholesterol-increasing effects, and monounsaturated FFAs were slightly reduced compared to the MCAo group, with some exceptions (eicosenoic-, eicosanoic-, and behenic acid). Such reduction has been reported to lower cholesterol and has neuroprotective effects, because the antioxidant properties play a role in the defense mechanisms against oxidative stress [18]. However, there was no significant difference in the levels of PUFAs in the MCAo and MCAo + hMSC groups.…”

Section: Discussionmentioning

confidence: 74%

“…The composition of free fatty acids (FFAs) is an important biochemical indicator of metabolic pathways in various pathological conditions [11][12][13][14]. In particular, changes in polyunsaturated fatty acid (PUFA) levels have been associated with the production of reactive oxygen species [15], destruction of the antioxidant system, and inflammation during ischemia [16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

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The free fatty acid metabolome in cerebral ischemia following human mesenchymal stem cell transplantation in rats

Paik

Ahn

et al. 2009

Clinica Chimica Acta

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

The free fatty acid metabolome in cerebral ischemia following human mesenchymal stem cell transplantation in rats

Paik

Ahn

et al. 2009

Clinica Chimica Acta

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“…The similar protective effects and PPAR ␥ activation can be produced by 15d-PGJ2, one of the AA-derived products via the cyclooxygenase pathway, treated during brain ischemia in vivo and in vitro ( 36,47,48 ). Even AA, from which 12(S)-and 15(S)-HETE are derived, has been shown to be neuroprotective against oxidative stress on hippocampal slices through a process involving PPAR ␥ signaling ( 33 ). Therefore, the PPAR ␥ -dependent mechanism is not selective for 12/15-LOX and its 12(S)-and 15(S)-HETE products.…”

Section: /15-lox-derived Metabolites 12(s)-and 15(s)-hetementioning

confidence: 92%

12/15-Lipoxygenase metabolites of arachidonic acid activate PPARγ: a possible neuroprotective effect in ischemic brain

Sun

Han

et al. 2015

Journal of Lipid Research

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This article is available online at http://www.jlr.org to form a series of biologically active lipid mediators ( 1, 2 ). In the CNS, 12/15-LOX expression has been described throughout the cerebrum, basal ganglia, and hippocampus ( 3, 4 ). Arachidonic acid (AA) is an important component of membrane lipids that can activate several signaling pathways directly by itself or by its metabolites ( 5 ). In nervous tissue, the major enzymatic route for AA metabolism is the 12/15-LOX pathway, and the principal metabolites are 12(S)-HETE and 15(S)-HETE ( 3, 4, 6, 7 ). The biological signifi cance of these metabolites of AA is that they have been proposed to play roles as second messengers in synaptic transmission and they are thought to be involved in learning and memory processes ( 8 ). In addition, 12(S)-HETE is known to act as an inhibitory neuromodulator by reducing voltage-sensitive calcium channel activity ( 9 ) and attenuating glutamate release and affi nity to its receptors ( 10-12 ).Brain ischemia triggers the massive release of free fatty acids from membrane stores, such as AA and DHA, and then the accumulation of lipid peroxides. 12/15-LOX is thought to be damaging because of its lipid-oxidizing properties, and the detrimental effects of 12/15-LOX have been documented by demonstrating the protection in the ischemic brain through 12/15-LOX inhibition or gene deletion ( 13-15 ). Several metabolites of 12/15-LOX, however, have neuroprotective and anti-infl ammatory qualities during brain ischemia. For example, 12/15-LOX metabolites derived from DHA and other -3 fatty acids inhibit cerebral ischemia-induced injury (16)(17)(18). This suggests 12/15-LOX and its metabolites may differ in their effects following cerebral ischemia.PPAR ␥ is a member of the nuclear hormone receptor family of ligand-dependent transcription factors. This work was supported by grants from the National Natural Science Foundation of China (number 81070968 to L.S. and number 81401023 to Y-W.X.) and from the Tianjin Municipal Science and Technology Commission (number 13ZCZDSY01900 to Y.C.). The authors declare no confl icts of interest. Manuscript received 15 July 2014 and in revised form 12(S)-and 15(S)-HETE activate PPAR ␥ in ischemic brain 503animals survived the MCAO surgical procedure. Rats that did not demonstrate neurological defi cits during 90 min MCAO were excluded from further study. Animals dying prematurely during the reperfusion period or having subarachnoid hemorrhage at postmortem examination were also excluded. Measurements derived from these animals were not included in the present study. Drug treatmentEicosanoids, 12(S)-HETE and 15(S)-HETE, were products of Cayman Chemical (Ann Arbor, MI) and given 30 min before the onset of MCAO by icv injection. 12(S)-and 15(S)-HETE, supplied in ethanol at 1 mg/ml, were air-dried under a stream of nitrogen and dissolved in a 30% DMSO and 70% isotonic saline solution ( 35 ). Animals received either vehicle (30% DMSO-0.9% saline) or a single dose of 12(S)-or 15(S)-HETE at 10, 15, or 20 g ( ‫...

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“…However, the effects of arachidonic acid on the viability of neurons are still somewhat controversial. Recently, Wang et al (2006) reported that arachidonic acid can effectively protect rat hippocampal neurons against oxidative stress induced by glutamate or H2O2 by enhancing antioxidative enzyme activities.…”

Section: Pufa and Brainmentioning

confidence: 99%

A putative link of PUFA, GPR40 and adult-born hippocampal neurons for memory

Yamashima

2008

Progress in Neurobiology

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Long chain polyunsaturated fatty acids (PUFA) such as docosahexaenoic and arachidonic acids, which are enriched in the brain, are important for multiple aspects of neuronal development and function including neurite outgrowth, signal transduction and membrane fluidity. Recent studies show that PUFA are capable of improving hippocampal long-term potentiation, learning ability of aged rats, and cognitive function of humans with memory deficits, although the underlying mechanisms are unknown.There have been several reports studying physiological roles of G-protein coupled receptor 40 (GPR40) in the pancreas, but no studies have focused on the function of GPR40 in the brain. As GPR40 was recently identified in neurons throughout the brain, it is probable that certain PUFA may act, as endogenous ligands, on GPR40 at their cell surface. However, the effects of PUFA upon neuronal functions are still not clearly understood. Here, although circumferential, a combination of in-vitro and in-vivo data is introduced to consider the effects of docosahexaenoic and arachidonic acids on brain functions. GPR40 was found in the newborn neurons of the normal and postischemic hippocampi of adult macaque monkeys, while the positive effects of PUFA upon Ca 2+ mobilization and cognitive functions were demonstrated in both GPR40 gene-transfected PC12 cells and human subjects with memory deficits. The purpose of this review is to propose a putative link among PUFA, GPR40, and hippocampal newborn neurons by discussing whether PUFA can improve memory functions through GPR40 activation of adult-born neurons. At present, little is known about PUFA requirements that make possible neurogenesis in the adult hippocampus. However, the idea that 'PUFA-GPR40 interaction might be crucial for adult neurogenesis and/or memory' should be examined in detail using various experimental paradigms.2

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Neuroprotective effects of arachidonic acid against oxidative stress on rat hippocampal slices

Cited by 110 publications

References 41 publications

The free fatty acid metabolome in cerebral ischemia following human mesenchymal stem cell transplantation in rats

The free fatty acid metabolome in cerebral ischemia following human mesenchymal stem cell transplantation in rats

12/15-Lipoxygenase metabolites of arachidonic acid activate PPARγ: a possible neuroprotective effect in ischemic brain

A putative link of PUFA, GPR40 and adult-born hippocampal neurons for memory

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