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Agmatine pretreatment protects retinal ganglion cells (RGC-5 cell line) from oxidative stress in vitro

Authors
 IIZUKA YOKO  ;  SAMIN HONG  ;  CHAN YUN KIM  ;  SEUNG KAB KIM  ;  GONG JE SEONG 
Citation
 BIOCELL, Vol.32(3) : 245-250, 2008 
Journal Title
BIOCELL
ISSN
 0327-9545 
Issue Date
2008
MeSH
Agmatine/pharmacology* ; Animals ; Apoptosis/drug effects ; Cell Differentiation/drug effects ; Cell Line ; Enzyme Inhibitors/pharmacology ; Neuroprotective Agents/pharmacology* ; Oxidative Stress/drug effects* ; Rats ; Retinal Ganglion Cells*/drug effects ; Retinal Ganglion Cells*/metabolism ; Staurosporine/pharmacology
Keywords
Neuronal damage ; Apoptosis ; Neuroprotection
Abstract
Agmatine, 2-(4-aminobutyl)guanidine, has been reported to have neuroprotective effects against various neuronal damages. In this study it was investigated whether agmatine pretreatment rescues the retinal ganglion cells from oxidative injury in vitro. After differentiation of transformed rat retinal ganglion cells (RGC-5 cell line) with staurosporine, agmatine (0.0 to 100.0 microM) pretreatment was performed for 2 hours. Subsequently, they were exposed to hydrogen peroxide (0.0 to 2.5 mM) as an oxidative stress. Cell viability was monitored for up to 48 hours with the lactate dehydrogenase (LDH) assay and apoptosis was examined by the terminal deoxynucleotide transferase-mediated terminal uridine deoxynucleotidyl transferase nick end-labeling (TUNEL) method. As a result, differentiated RGC-5 cells were found to have decreased viability after addition of hydrogen peroxide in a dose-dependent manner. This hydrogen peroxide induced cytotoxicity caused apoptosis characterized by DNA fragmentation. Agmatine pretreatment not only increased cell viability but also attenuated DNA fragmentation. In conclusion, agmatine pretreatment demonstrated neuroprotective effects against oxidative stress induced by hydrogen peroxide in differentiated RGC-5 cells in vitro. This suggests a novel therapeutic strategy rescuing retinal ganglion cells from death caused by oxidative injury.
Full Text
http://www.scielo.org.ar/scielo.php?pid=S0327-95452008000300005&script=sci_arttext
DOI
19181187
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Chan Yun(김찬윤) ORCID logo https://orcid.org/0000-0002-8373-9999
Seong, Gong Je(성공제) ORCID logo https://orcid.org/0000-0002-5456-4296
Hong, Sa Min(홍사민)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/108349
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