Acetyl-l-carnitine rescues scopolamine-induced memory deficits by restoring insulin-like growth factor II via decreasing p53 oxidation

Xiang, Wu; Wang, Liangping; Tang, Hui; Shan, Wanying; Wang, Xiong; Liú, Dan; Tian, Qing; Wang, Jian‐Zhi; Zhu, Ling‐Qiang

doi:10.1016/j.neuropharm.2013.08.022

Cited by 30 publications

(9 citation statements)

References 68 publications

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“…Previous reports found that etomidate acts on GABAergic neurons to exert its anesthetic activity,[ 22 ] and GABAergic neurons are known to be particularly susceptible to oxidative stress. [ 23 ] Therefore, the lack of change in the oxidative stress parameters observed here was reasonable and consistent with a previous study. [ 24 ]…”

Section: Discussionsupporting

confidence: 93%

Underlying Mechanisms of Memory Deficits Induced by Etomidate Anesthesia in Aged Rat Model

Wei

et al. 2016

Chinese Medical Journal

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Background:Etomidate (R-1-[1-ethylphenyl] imidazole-5-ethyl ester) is a widely used anesthetic drug that had been reported to contribute to cognitive deficits after general surgery. However, its underlying mechanisms have not been fully elucidated. In this study, we aimed to explore the neurobiological mechanisms of cognitive impairments that caused by etomidate.Methods:A total of 30 Sprague-Dawley rats were used and divided into two groups randomly to receive a single injection of etomidate or vehicle. Then, the rats’ spatial memory ability and neuronal survival were evaluated using the Morris water maze test and Nissl staining, respectively. Furthermore, we analyzed levels of oxidative stress, as well as cyclic adenosine 3’,5’-monophosphate response element-binding (CREB) protein phosphorylation and immediate early gene (IEG, including Arc, c-fos, and Egr1) expression levels using Western blot analysis.Results:Compared with vehicle-treated rats, the etomidate-treated rats displayed impaired spatial learning (day 4: 27.26 ± 5.33 s vs. 35.52 ± 3.88 s, t = 2.988, P = 0.0068; day 5: 15.84 ± 4.02 s vs. 30.67 ± 4.23 s, t = 3.013, P = 0.0057; day 6: 9.47 ± 2.35 s vs. 25.66 ± 4.16 s, t = 3.567, P = 0.0036) and memory ability (crossing times: 4.40 ± 1.18 vs. 2.06 ± 0.80, t = 2.896, P = 0.0072; duration: 34.00 ± 4.24 s vs. 18.07 ± 4.79 s, t = 3.023, P = 0.0053; total swimming distance: 40.73 ± 3.45 cm vs. 27.40 ± 6.56 cm, t = 2.798, P = 0.0086) but no neuronal death. Furthermore, etomidate did not cause oxidative stress or deficits in CREB phosphorylation. The levels of multiple IEGs (Arc: vehicle treated rats 100%, etomidate treated rats 86%, t = 2.876, P = 0.0086; c-fos: Vehicle treated rats 100%, etomidate treated rats 72%, t = 2.996, P = 0.0076; Egr1: Vehicle treated rats 100%, etomidate treated rats 58%, t = 3.011, P = 0.0057) were significantly reduced in hippocampi of etomidate-treated rats.Conclusion:Our data suggested that etomidate might induce memory impairment in rats via inhibition of IEG expression.

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Section: Discussionsupporting

confidence: 93%

Underlying Mechanisms of Memory Deficits Induced by Etomidate Anesthesia in Aged Rat Model

Wei

et al. 2016

Chinese Medical Journal

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“…Generally, acetylcarnitine is considered as a neuroprotective agent, which could suppress the phosphorylation of beta-amyloid precursor proteins, protect neuron cells against lipid peroxidation, reduce apoptosis and increase nerve growth factor production [33,34]. Both human and animal experiments reported acetylcarnitine could ameliorate AD progress and enhance memory ability [35][36][37]. A decreased level of acetylcarnitine was observed in most brain regions of AD patient [38], which is in accord with model group in our experiment.…”

Section: Discussionsupporting

confidence: 86%

A UHPLC–TOF/MS method based metabonomic study of total ginsenosides effects on Alzheimer disease mouse model

Gong

Liu

Zhou

et al. 2015

Journal of Pharmaceutical and Biomedical Analysis

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“…Testing hypotheses related to these differential correlations is not straightforward. If we observe levels in a single metabolite that are associated with a trait of interest, we can try to increase or decrease levels of that metabolite through genetic (Eisenberg et al ., 2014 ) or pharmacological (Wang et al ., 2014 ) means. More challenging still, it remains to be seen whether we can alter age-related changes in metabolite correlations by feeding two or more metabolites to flies simultaneously, or altering expression patterns of multiple enzymes associated with metabolites whose correlations change with age.…”

Section: Discussionmentioning

confidence: 99%

The effects of age and dietary restriction on the tissue‐specific metabolome of Drosophila

et al. 2015

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Dietary restriction (DR) is a robust intervention that extends lifespan and slows the onset of age-related diseases in diverse organisms. While significant progress has been made in attempts to uncover the genetic mechanisms of DR, there are few studies on the effects of DR on the metabolome. In recent years, metabolomic profiling has emerged as a powerful technology to understand the molecular causes and consequences of natural aging and disease-associated phenotypes. Here, we use high-resolution mass spectroscopy and novel computational approaches to examine changes in the metabolome from the head, thorax, abdomen, and whole body at multiple ages in Drosophila fed either a nutrient-rich ad libitum (AL) or nutrient-restricted (DR) diet. Multivariate analysis clearly separates the metabolome by diet in different tissues and different ages. DR significantly altered the metabolome and, in particular, slowed age-related changes in the metabolome. Interestingly, we observed interacting metabolites whose correlation coefficients, but not mean levels, differed significantly between AL and DR. The number and magnitude of positively correlated metabolites was greater under a DR diet. Furthermore, there was a decrease in positive metabolite correlations as flies aged on an AL diet. Conversely, DR enhanced these correlations with age. Metabolic set enrichment analysis identified several known (e.g., amino acid and NAD metabolism) and novel metabolic pathways that may affect how DR effects aging. Our results suggest that network structure of metabolites is altered upon DR and may play an important role in preventing the decline of homeostasis with age.

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Acetyl-l-carnitine rescues scopolamine-induced memory deficits by restoring insulin-like growth factor II via decreasing p53 oxidation

Cited by 30 publications

References 68 publications

Underlying Mechanisms of Memory Deficits Induced by Etomidate Anesthesia in Aged Rat Model

Underlying Mechanisms of Memory Deficits Induced by Etomidate Anesthesia in Aged Rat Model

A UHPLC–TOF/MS method based metabonomic study of total ginsenosides effects on Alzheimer disease mouse model

The effects of age and dietary restriction on the tissue‐specific metabolome of Drosophila

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