ArticleNeuroscience2009
Activity-dependent neuroprotective protein-derived peptide, NAP, preventing alcohol-induced apoptosis in fetal brain of C57BL/6 mouse.
Article in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- Targeting Tau to Treat Clinical Features of Huntington's Disease.Frontiers in neurology · 2020Review
- Effects of prenatal alcohol exposure (PAE): insights into FASD using mouse models of PAE.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2018Review
- Prenatal alcohol-induced neuroapoptosis in rat brain cerebral cortex: protective effect of folic acid and betaine.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2017Article
- Experimental methods for testing the effects of neurotrophic peptide, ADNF-9, against alcohol-induced apoptosis during pregnancy in c57bl/6 mice.Journal of visualized experiments : JoVE · 2013Article
- Neurotrophic peptides, ADNF-9 and NAP, prevent alcohol-induced apoptosis at midgestation in fetal brains of C57BL/6 mouse.Journal of molecular neuroscience : MN · 2013Article
- Article
- Tau and caspase 3 as targets for neuroprotection.International journal of Alzheimer's disease · 2012Article
- Neuroprotective peptide ADNF-9 in fetal brain of C57BL/6 mice exposed prenatally to alcohol.Journal of biomedical science · 2011Article
- Potential drugs and methods for preventing or delaying the progression of Huntington's disease.Recent patents on CNS drug discovery · 2011Article
- Prenatal choline supplementation mitigates behavioral alterations associated with prenatal alcohol exposure in rats.Birth defects research. Part A, Clinical and molecular teratology · 2010Article
- Alteration of selective neurotransmitters in fetal brains of prenatally alcohol-treated C57BL/6 mice: quantitative analysis using liquid chromatography/tandem mass spectrometry.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2010Article
- The neuroprotective peptide NAP does not directly affect polymerization or dynamics of reconstituted neural microtubules.Journal of Alzheimer's disease : JAD · 2010Article
- Differential expression of proteins in fetal brains of alcohol-treated prenatally C57BL/6 mice: a proteomic investigation.Electrophoresis · 2010Article
- A novel peptide, colivelin, prevents alcohol-induced apoptosis in fetal brain of C57BL/6 mice: signaling pathway investigations.Neuroscience · 2009Article
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Authors and funding
1 author at 1 institution in 1 country.
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Abstract
Possible prevention of the effects of prenatal alcohol exposure has been investigated using peptides that were previously shown to be involved in neuroprotection both in vitro and in vivo. I focused in this study on investigating the neuroprotective effects of one of these peptides with regard to the determination of the downstream signaling pathways involved in neuroprotection. This peptide with the sequence NAPVSIPQ, known as NAP, a fragment of activity-dependent neuroprotective protein, demonstrated a potent protective effect against oxidative stress associated with alcohol exposure. On embryonic day 7 (E7), weight-matched C57BL/6 pregnant females were assigned the following groups: (1) Ethanol liquid diet group (ALC) 25% (4.49%, v/v) ethano-derived calories, (2) Pair-fed (PF) control group (3) Chow control group, (4) treatment groups with alcohol alongside i.p. injections of d-NAP (ALC/d-NAP, 20 or 30 microg/20 g body weight), (5) PF/d-NAP control group. On E13, fetal brains were collected and assayed for TdT-mediated dUTP nick end labeling (TUNEL) staining, caspase-3 colorimetric assay and ELISA for cytochrome c detection. My results show that NAP significantly prevented alcohol-induced weight reduction of the fetal brain. Apoptosis was determined by TUNEL staining; NAP administration significantly prevented alcohol-induced increases in TUNEL-positive cells in primordium cingulate cortex and basal ganglia eminence. The investigation of downstream signaling pathways involving NAP neuroprotection revealed that this peptide significantly prevented alcohol-induced increase in the concentrations of caspase-3 in E13 fetal brains. Moreover, ELISA for cytochrome c shows that NAP significantly prevented both alcohol-induced increases in the level of cytosolic cytochrome c and alcohol-induced decreases in the level of mitochondrial cytochrome c. These data provide an understanding of NAP intracellular target, and the downstream mechanisms of action that will pave a path toward potential therapeutics against alcohol intoxication during prenatal stages.
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