glycyl-prolyl-glutamic-acid and glycyl-prolyl-arginine

glycyl-prolyl-glutamic-acid has been researched along with glycyl-prolyl-arginine* in 1 studies

Other Studies

1 other study(ies) available for glycyl-prolyl-glutamic-acid and glycyl-prolyl-arginine

Article	Year
A three amino acid peptide, Gly-Pro-Arg, protects and rescues cell death induced by amyloid beta-peptide. Experimental neurology, 2003, Volume: 184, Issue:2 Amyloid beta-peptide (Abeta) contributes to the pathogenesis of Alzheimer's disease (AD), causing neuronal death through apoptosis. In this study, the neuroprotective role of small peptides, Gly-Pro-Glu (GPE), Gly-Glu (GE), Gly-Pro-Asp (GPD), and Gly-Pro-Arg (GPR) were examined against Abeta-induced toxicity in cultured rat hippocampal neurons. We report here that GPR (10-100 microM) prevented Abeta-mediated increase in lactate dehydrogenase (LDH) release and Abeta inhibition of MTT reduction, even in neurons that were pre-exposed to Abeta for 24 or 48 h. Since GPR prevented Abeta inhibition of MTT reduction, the anti-apoptotic effect of GPR was studied by examining activation of caspase-3 and expression of p53 protein. Caspase-3 was significantly activated by 20 microM Abeta25-35 and 5 microM Abeta1-40, but GPR effectively prevented the Abeta-mediated activation of caspase-3. Similarly, Abeta increased numbers of p53-positive cells, but GPR prevented this Abeta effect. Our findings suggest that GPR can rescue cultured rat hippocampal neurons from Abeta-induced neuronal death by inhibiting caspase-3/p53-dependent apoptosis. Topics: Amyloid beta-Peptides; Animals; Apoptosis; Caspase 3; Caspases; Cells, Cultured; Dipeptides; Enzyme Activation; Hippocampus; Immunohistochemistry; L-Lactate Dehydrogenase; Neurons; Neuroprotective Agents; Oligopeptides; Rats; Rats, Sprague-Dawley; Tetrazolium Salts; Thiazoles; Tumor Suppressor Protein p53	2003

Article

Year

A three amino acid peptide, Gly-Pro-Arg, protects and rescues cell death induced by amyloid beta-peptide.

Experimental neurology, 2003, Volume: 184, Issue:2

Amyloid beta-peptide (Abeta) contributes to the pathogenesis of Alzheimer's disease (AD), causing neuronal death through apoptosis. In this study, the neuroprotective role of small peptides, Gly-Pro-Glu (GPE), Gly-Glu (GE), Gly-Pro-Asp (GPD), and Gly-Pro-Arg (GPR) were examined against Abeta-induced toxicity in cultured rat hippocampal neurons. We report here that GPR (10-100 microM) prevented Abeta-mediated increase in lactate dehydrogenase (LDH) release and Abeta inhibition of MTT reduction, even in neurons that were pre-exposed to Abeta for 24 or 48 h. Since GPR prevented Abeta inhibition of MTT reduction, the anti-apoptotic effect of GPR was studied by examining activation of caspase-3 and expression of p53 protein. Caspase-3 was significantly activated by 20 microM Abeta25-35 and 5 microM Abeta1-40, but GPR effectively prevented the Abeta-mediated activation of caspase-3. Similarly, Abeta increased numbers of p53-positive cells, but GPR prevented this Abeta effect. Our findings suggest that GPR can rescue cultured rat hippocampal neurons from Abeta-induced neuronal death by inhibiting caspase-3/p53-dependent apoptosis.

Topics: Amyloid beta-Peptides; Animals; Apoptosis; Caspase 3; Caspases; Cells, Cultured; Dipeptides; Enzyme Activation; Hippocampus; Immunohistochemistry; L-Lactate Dehydrogenase; Neurons; Neuroprotective Agents; Oligopeptides; Rats; Rats, Sprague-Dawley; Tetrazolium Salts; Thiazoles; Tumor Suppressor Protein p53

2003