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

Y. Iizuka, Samin Hong, C. Kim, S. Kim, G. Seong
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引用次数: 22

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.
胍丁胺预处理对视网膜神经节细胞(RGC-5细胞系)氧化应激的保护作用。
胍丁氨酸,2-(4-氨基丁基)胍,已被报道对各种神经损伤具有神经保护作用。本研究探讨了胍丁胺预处理是否能在体外修复视网膜神经节细胞的氧化损伤。转化后的大鼠视网膜神经节细胞(RGC-5细胞系)经staurosporine分化后,agmatine(0.0 ~ 100.0微米)预处理2小时。随后,将它们暴露于过氧化氢(0.0至2.5 mM)中作为氧化应激。采用乳酸脱氢酶(LDH)法监测细胞活力长达48小时,采用末端脱氧核苷酸转移酶介导的末端尿苷脱氧核苷酸转移酶缺口末端标记(TUNEL)法检测细胞凋亡。结果发现,在加入过氧化氢后,分化的RGC-5细胞的活力呈剂量依赖性下降。过氧化氢诱导细胞毒性导致以DNA断裂为特征的细胞凋亡。Agmatine预处理不仅能提高细胞活力,还能减弱DNA断裂。综上所述,胍丁胺预处理对体外分化的RGC-5细胞具有抗过氧化氢氧化应激的神经保护作用。这提示了一种新的治疗策略,可以挽救氧化损伤引起的视网膜神经节细胞死亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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