普瑞巴林保护顺铂诱导的神经细胞系氧化神经毒性

Q4 Biochemistry, Genetics and Molecular Biology

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2019-06-18 DOI:10.37212/jcnos.653500

Kemal Ertilav

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引用次数: 10

摘要

顺铂(CSP)用于治疗几种癌症。然而，它也通过过量的活性氧产生和激活神经元中的TRPV1通道激活而产生不良影响。普瑞巴林(PGAB)对神经元具有抗氧化和钙通道阻断作用。我研究了PGAB对DBTRG神经元细胞CSP不良反应的保护作用。将神经元细胞分为4组，分别为对照组、PGAB组(500M)、CSP组(25M)、PGAB+CSP联合组(24 h)。经PGAB处理后，cisp诱导的神经元细胞活力降低，细胞内谷胱甘肽过氧化物酶和谷胱甘肽水平升高。然而，PGAB处理后，csp诱导的细胞凋亡、Ca2+荧光强度、TRPV1电流密度通过线粒体氧化应激的增加而降低。综上所述，在PGAB的作用下，csp诱导的神经元细胞线粒体ROS的增加和细胞死亡水平的降低是通过降低TRPV1的激活来实现的。PGAB可减轻csp诱导的神经元耐药。

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Pregabalin protected cisplatin-induced oxidative neurotoxicity in neuronal cell line

Cisplatin (CSP) is used treatment of several cancers. However, it has also adverse effect through excessive reactive oxygen species production and activation of TRPV1 channel activation in neurons. Pregabalin (PGAB) has antioxidant and calcium channel blocker actions in neurons. I have investigated protective role of PGAB against the adverse effects of CSP in DBTRG neuronal cells. The neuronal cells were divided into four groups as control group, PGAB group (500 M for 24 1 hrs), CSP group (25 M for 24 hrs), and PGAB+CSP combination group. CISP-induced decrease of cell viability, glutathione peroxidase and glutathione level in the cells were increased in the neurons by PGAB treatment. However, CSP-induced increase of apoptosis, Ca2+ fluorescence intensity, TRPV1 current densities through the increase mitochondrial oxidative stress were decreased in the neurons by PGAB treatment. In conclusion, CSP-induced increases in mitochondrial ROS and cell death levels in the neuronal cells were decreased through the decrease of TRPV1 activation with the effect of PGAB treatment. CSP-induced drug resistance in the neurons might be reduced by PGAB treatment.

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来源期刊

Journal of Cellular Neuroscience and Oxidative Stress Biochemistry, Genetics and Molecular Biology-Biophysics

CiteScore

1.10

自引率

0.00%

发文量

期刊介绍： Journal of Cellular Neuroscience and Oxidative Stress isan online journal that publishes original research articles, reviews and short reviews on themolecular basisofbiophysical,physiological and pharmacological processes thatregulate cellular function, and the control or alteration of these processesby theaction of receptors, neurotransmitters, second messengers, cation, anions,drugsor disease. Areas of particular interest are four topics. They are; 1. Ion Channels (Na+-K+Channels, Cl– channels, Ca2+channels, ADP-Ribose and metabolism of NAD+,Patch-Clamp applications) 2. Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) 3. Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD+ on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson’s and Alzheimer’s diseases) 4. Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)