Open Access

ARTICLE

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

by IIZUKA YOKO, SAMIN HONG, CHAN YUN KIM, SEUNG KAB KIM, GONG JE SEONG

1. Brain Korea 21 Project for Medical Science, Yonsei University, Seoul, Korea
2. Institute of Vision Research, Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea.
Address correspondence to: Gong Je Seong. Department of Ophthalmology, Yongdong Severance Hospital, Yonsei University College of Medicine, 612 Eonjuro, Gangnamgu, Seoul 135-720, Republic of Korea. E-mail: gjseong@yuhs.ac

BIOCELL 2008, 32(3), 245-250. https://doi.org/10.32604/biocell.2008.32.245

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 μM) 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

---

Keywords

---

Citations