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The neuroprotective effect of agmatine against amyloid β-induced apoptosis in primary cultured hippocampal cells involving ERK, Akt/GSK-3β, and TNF-α.
Mol Biol Rep. 2019 Feb; 46(1):489-496.MB

Abstract

β-Amyloid peptide (Aβ), the major element of senile plaques in Alzheimer's disease (AD), has been found to accumulate in brain regions critical for memory and cognition. Deposits of Aβ trigger neurotoxic events which lead to neural apoptotic death. The present study examined whether agmatine, an endogenous polyamine formed by the decarboxylation of L-arginine, possesses a neuroprotective effect against Aβ-induced toxicity. Primary rat hippocampal cells extracted from the brains of 18-19-day-old embryos were exposed to 10 µM of Aβ (25-35) in the absence or presence of agmatine at 150 or 250 µM. Additionally, the involvement of Akt (Protein Kinae B), GSK-3β (glycogen synthase kinase 3-β), ERK (Extracellular Signal-Regulated Kinase) and TNF-α (Tumor necrosis factor-α) in the agmatine protection against Aβ-induced neurotoxicity was investigated. Agmatine significantly prevented the effect of Aβ exposure on cell viability and caspase-3 assays. Furthermore, agmatine considerably restored Aβ-induced decline of phospho-Akt and phospho-GSK and blocked Aβ-induced increase of phospho-ERK and TNF-alpha. Taken together, these findings might shed light on the protective effect of agmatine as a potential therapeutic agent for AD.

Authors+Show Affiliations

Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.Department of Physiology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Neurophysiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.Department of Physiology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Neurophysiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.Shiraz Nuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. marmoosavi@sums.ac.ir. Nanobiology and Nanomedicine Research Centre, Shiraz University of Medical sciences, Shiraz, Iran. marmoosavi@sums.ac.ir.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30474774

Citation

Hooshmandi, Etrat, et al. "The Neuroprotective Effect of Agmatine Against Amyloid Β-induced Apoptosis in Primary Cultured Hippocampal Cells Involving ERK, Akt/GSK-3β, and TNF-α." Molecular Biology Reports, vol. 46, no. 1, 2019, pp. 489-496.
Hooshmandi E, Ghasemi R, Iloun P, et al. The neuroprotective effect of agmatine against amyloid β-induced apoptosis in primary cultured hippocampal cells involving ERK, Akt/GSK-3β, and TNF-α. Mol Biol Rep. 2019;46(1):489-496.
Hooshmandi, E., Ghasemi, R., Iloun, P., & Moosavi, M. (2019). The neuroprotective effect of agmatine against amyloid β-induced apoptosis in primary cultured hippocampal cells involving ERK, Akt/GSK-3β, and TNF-α. Molecular Biology Reports, 46(1), 489-496. https://doi.org/10.1007/s11033-018-4501-4
Hooshmandi E, et al. The Neuroprotective Effect of Agmatine Against Amyloid Β-induced Apoptosis in Primary Cultured Hippocampal Cells Involving ERK, Akt/GSK-3β, and TNF-α. Mol Biol Rep. 2019;46(1):489-496. PubMed PMID: 30474774.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The neuroprotective effect of agmatine against amyloid β-induced apoptosis in primary cultured hippocampal cells involving ERK, Akt/GSK-3β, and TNF-α. AU - Hooshmandi,Etrat, AU - Ghasemi,Rasoul, AU - Iloun,Parisa, AU - Moosavi,Maryam, Y1 - 2018/11/24/ PY - 2018/08/25/received PY - 2018/11/13/accepted PY - 2018/11/27/pubmed PY - 2019/7/3/medline PY - 2018/11/27/entrez KW - Agmatine KW - Akt/GSK3β KW - Beta amyloid KW - ERK KW - Hippocampal cell culture KW - TNF-α SP - 489 EP - 496 JF - Molecular biology reports JO - Mol. Biol. Rep. VL - 46 IS - 1 N2 - β-Amyloid peptide (Aβ), the major element of senile plaques in Alzheimer's disease (AD), has been found to accumulate in brain regions critical for memory and cognition. Deposits of Aβ trigger neurotoxic events which lead to neural apoptotic death. The present study examined whether agmatine, an endogenous polyamine formed by the decarboxylation of L-arginine, possesses a neuroprotective effect against Aβ-induced toxicity. Primary rat hippocampal cells extracted from the brains of 18-19-day-old embryos were exposed to 10 µM of Aβ (25-35) in the absence or presence of agmatine at 150 or 250 µM. Additionally, the involvement of Akt (Protein Kinae B), GSK-3β (glycogen synthase kinase 3-β), ERK (Extracellular Signal-Regulated Kinase) and TNF-α (Tumor necrosis factor-α) in the agmatine protection against Aβ-induced neurotoxicity was investigated. Agmatine significantly prevented the effect of Aβ exposure on cell viability and caspase-3 assays. Furthermore, agmatine considerably restored Aβ-induced decline of phospho-Akt and phospho-GSK and blocked Aβ-induced increase of phospho-ERK and TNF-alpha. Taken together, these findings might shed light on the protective effect of agmatine as a potential therapeutic agent for AD. SN - 1573-4978 UR - https://www.unboundmedicine.com/medline/citation/30474774/The_neuroprotective_effect_of_agmatine_against_amyloid_β_induced_apoptosis_in_primary_cultured_hippocampal_cells_involving_ERK_Akt/GSK_3β_and_TNF_α_ L2 - https://doi.org/10.1007/s11033-018-4501-4 DB - PRIME DP - Unbound Medicine ER -