N-acetyl-L-cysteine amide protects retinal pigment epithelium against methamphetamine-induced oxidative stress

J. W. Carey, Shakila Tobwala, Xinsheng Zhang, Atrayee Banerjee, N. Ercal, E. Pınarcı, H. Karacal
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引用次数: 9

Abstract

Methamphetamine (METH), a highly addictive drug used worldwide, induces oxidative stress in various animal organs. Recent animal studies indicate that methamphetamine also induces oxidative stress in the retina, which is an embryonic extension of the forebrain. The aim of this study, therefore, was to evaluate the protecttive effects of N-acetylcysteine amide (NACA) against oxidative stress induced by METH in retinal pigment epithelium (RPE) cells. Our studies showed that NACA protected against METH-induced oxidative stress in retinal pigment epithelial cells. Although METH significantly decreased glutathione (GSH) levels and increased reactive oxygen species (ROS) and malondialdehyde (MDA) levels, these returned to control levels with NACA treatment. Overall observations indicated that NACA protected RPE cells against oxidative cell damage and death by inhibiting lipid peroxidation, scavenging ROS, increasing levels of intracellular GSH, and maintaining the antioxidant enzyme activity and the integrity of the bloodretinal barrier (BRB). The effectiveness of NACA should be further evaluated to determine its potential for the treatment of numerous retinal diseases caused by oxidative stress.
n -乙酰- l-半胱氨酸酰胺保护视网膜色素上皮免受甲基苯丙胺诱导的氧化应激
甲基苯丙胺(Methamphetamine,简称冰毒)是一种在世界范围内使用的高度成瘾性药物,它会引起动物各种器官的氧化应激。最近的动物研究表明,甲基苯丙胺也会引起视网膜的氧化应激,视网膜是前脑的胚胎延伸。因此,本研究的目的是评估n -乙酰半胱氨酸酰胺(NACA)对甲基安非他明诱导的视网膜色素上皮(RPE)细胞氧化应激的保护作用。我们的研究表明,NACA可以保护视网膜色素上皮细胞免受甲基苯丙胺诱导的氧化应激。虽然甲基苯丙胺显著降低谷胱甘肽(GSH)水平,增加活性氧(ROS)和丙二醛(MDA)水平,但在NACA处理后,这些水平恢复到对照水平。总体观察结果表明,NACA通过抑制脂质过氧化、清除ROS、增加细胞内GSH水平、维持抗氧化酶活性和血视网膜屏障(BRB)的完整性,保护RPE细胞免受氧化性细胞损伤和死亡。应进一步评估NACA的有效性,以确定其治疗由氧化应激引起的多种视网膜疾病的潜力。
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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