Neuroprotective effects of agmatine on oxygen-glucose deprived primary-cultured astrocytes and nuclear translocation of nuclear factor-kappa B

Won Taek Lee, Samin Hong, Sung Hwan Yoon, Jae Hwan Kim, Kyung Ah Park, Gong Je Seong, Jongeun Lee

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

To better understand the neuroprotective actions of agmatine in ischemic insults, its effects on astrocytes were investigated using an in vitro oxygen-glucose deprivation (OGD) model. After primary culture, cortical astrocytes were moved into a closed anaerobic chamber and incubated in glucose-free culture media. 4 h later, the cells were restored to normoxic conditions and supplied with glucose for 20 h. The ability of agmatine to rescue astrocytes from OGD only and OGD followed by restoration (OGD-R) was assessed. Cell viability was monitored with or without 100 μM agmatine, using the lactate dehydrogenase (LDH) assay and annexin V flow cytometric assay. For morphological analysis, Hoechst 33258 and propidium iodide double nuclear staining was performed. Expression and phosphorylation of nuclear factor-kappa B (NF-κB) family proteins were also investigated by immunoblotting. Results showed that astrocytes had decreased viability following OGD and OGD-R and that agmatine treatment increased cell viability and induced NF-κB translocation into the nucleus. Finally, our studies revealed that agmatine can rescue astrocytes from death caused by ischemic and/or ischemic-perfusion neuronal injuries in vitro. Our findings provide new insights that may lead to a novel therapeutic strategy to reduce these kinds of neuronal injuries.

Original languageEnglish
Pages (from-to)64-70
Number of pages7
JournalBrain Research
Volume1281
DOIs
Publication statusPublished - 2009 Jul 24

Fingerprint

Agmatine
NF-kappa B
Neuroprotective Agents
Astrocytes
Oxygen
Glucose
Cell Survival
Bisbenzimidazole
Propidium
Annexin A5
Wounds and Injuries
L-Lactate Dehydrogenase
Immunoblotting
Culture Media
Perfusion
Phosphorylation
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Clinical Neurology
  • Developmental Biology
  • Molecular Biology

Cite this

Lee, Won Taek ; Hong, Samin ; Yoon, Sung Hwan ; Kim, Jae Hwan ; Park, Kyung Ah ; Seong, Gong Je ; Lee, Jongeun. / Neuroprotective effects of agmatine on oxygen-glucose deprived primary-cultured astrocytes and nuclear translocation of nuclear factor-kappa B. In: Brain Research. 2009 ; Vol. 1281. pp. 64-70.
@article{0e1b5e4410914d1c99050c3ff201974f,
title = "Neuroprotective effects of agmatine on oxygen-glucose deprived primary-cultured astrocytes and nuclear translocation of nuclear factor-kappa B",
abstract = "To better understand the neuroprotective actions of agmatine in ischemic insults, its effects on astrocytes were investigated using an in vitro oxygen-glucose deprivation (OGD) model. After primary culture, cortical astrocytes were moved into a closed anaerobic chamber and incubated in glucose-free culture media. 4 h later, the cells were restored to normoxic conditions and supplied with glucose for 20 h. The ability of agmatine to rescue astrocytes from OGD only and OGD followed by restoration (OGD-R) was assessed. Cell viability was monitored with or without 100 μM agmatine, using the lactate dehydrogenase (LDH) assay and annexin V flow cytometric assay. For morphological analysis, Hoechst 33258 and propidium iodide double nuclear staining was performed. Expression and phosphorylation of nuclear factor-kappa B (NF-κB) family proteins were also investigated by immunoblotting. Results showed that astrocytes had decreased viability following OGD and OGD-R and that agmatine treatment increased cell viability and induced NF-κB translocation into the nucleus. Finally, our studies revealed that agmatine can rescue astrocytes from death caused by ischemic and/or ischemic-perfusion neuronal injuries in vitro. Our findings provide new insights that may lead to a novel therapeutic strategy to reduce these kinds of neuronal injuries.",
author = "Lee, {Won Taek} and Samin Hong and Yoon, {Sung Hwan} and Kim, {Jae Hwan} and Park, {Kyung Ah} and Seong, {Gong Je} and Jongeun Lee",
year = "2009",
month = "7",
day = "24",
doi = "10.1016/j.brainres.2009.05.046",
language = "English",
volume = "1281",
pages = "64--70",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",

}

Neuroprotective effects of agmatine on oxygen-glucose deprived primary-cultured astrocytes and nuclear translocation of nuclear factor-kappa B. / Lee, Won Taek; Hong, Samin; Yoon, Sung Hwan; Kim, Jae Hwan; Park, Kyung Ah; Seong, Gong Je; Lee, Jongeun.

In: Brain Research, Vol. 1281, 24.07.2009, p. 64-70.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Neuroprotective effects of agmatine on oxygen-glucose deprived primary-cultured astrocytes and nuclear translocation of nuclear factor-kappa B

AU - Lee, Won Taek

AU - Hong, Samin

AU - Yoon, Sung Hwan

AU - Kim, Jae Hwan

AU - Park, Kyung Ah

AU - Seong, Gong Je

AU - Lee, Jongeun

PY - 2009/7/24

Y1 - 2009/7/24

N2 - To better understand the neuroprotective actions of agmatine in ischemic insults, its effects on astrocytes were investigated using an in vitro oxygen-glucose deprivation (OGD) model. After primary culture, cortical astrocytes were moved into a closed anaerobic chamber and incubated in glucose-free culture media. 4 h later, the cells were restored to normoxic conditions and supplied with glucose for 20 h. The ability of agmatine to rescue astrocytes from OGD only and OGD followed by restoration (OGD-R) was assessed. Cell viability was monitored with or without 100 μM agmatine, using the lactate dehydrogenase (LDH) assay and annexin V flow cytometric assay. For morphological analysis, Hoechst 33258 and propidium iodide double nuclear staining was performed. Expression and phosphorylation of nuclear factor-kappa B (NF-κB) family proteins were also investigated by immunoblotting. Results showed that astrocytes had decreased viability following OGD and OGD-R and that agmatine treatment increased cell viability and induced NF-κB translocation into the nucleus. Finally, our studies revealed that agmatine can rescue astrocytes from death caused by ischemic and/or ischemic-perfusion neuronal injuries in vitro. Our findings provide new insights that may lead to a novel therapeutic strategy to reduce these kinds of neuronal injuries.

AB - To better understand the neuroprotective actions of agmatine in ischemic insults, its effects on astrocytes were investigated using an in vitro oxygen-glucose deprivation (OGD) model. After primary culture, cortical astrocytes were moved into a closed anaerobic chamber and incubated in glucose-free culture media. 4 h later, the cells were restored to normoxic conditions and supplied with glucose for 20 h. The ability of agmatine to rescue astrocytes from OGD only and OGD followed by restoration (OGD-R) was assessed. Cell viability was monitored with or without 100 μM agmatine, using the lactate dehydrogenase (LDH) assay and annexin V flow cytometric assay. For morphological analysis, Hoechst 33258 and propidium iodide double nuclear staining was performed. Expression and phosphorylation of nuclear factor-kappa B (NF-κB) family proteins were also investigated by immunoblotting. Results showed that astrocytes had decreased viability following OGD and OGD-R and that agmatine treatment increased cell viability and induced NF-κB translocation into the nucleus. Finally, our studies revealed that agmatine can rescue astrocytes from death caused by ischemic and/or ischemic-perfusion neuronal injuries in vitro. Our findings provide new insights that may lead to a novel therapeutic strategy to reduce these kinds of neuronal injuries.

UR - http://www.scopus.com/inward/record.url?scp=67649394099&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67649394099&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2009.05.046

DO - 10.1016/j.brainres.2009.05.046

M3 - Article

C2 - 19465011

AN - SCOPUS:67649394099

VL - 1281

SP - 64

EP - 70

JO - Brain Research

JF - Brain Research

SN - 0006-8993

ER -