Potent antioxidant alpha lipoic acid reduces STZ-induced oxidative stress and apoptosis levels in the erythrocytes and brain cells of diabetic rats

Q4 Biochemistry, Genetics and Molecular Biology

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2023-01-31 DOI:10.37212/jcnos.1245152

Betul Yazğan, Y. Yazğan

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引用次数: 2

Abstract

Diabetes, which causes oxidative stress-induced neuronal damage, is still one of the most important chronic health problems in the world. It can cause serious cellular loss and damage throughout the course of the disease. It is hypothesized that increased oxidative stress in this process increases free reactive oxygen species (ROS) and apoptotic markers and causes diabetic damage. Alpha-Lipoic acid (α-LA), which has a direct antioxidant effect in ROS reduction reactions, is also among the main components of the antioxidant system that works for free radical control and apoptosis. To understand the role of α-LA in reducing diabetes-induced oxidative damage, we examined the production of ROS in the brain cortex and erythrocytes of rats and their effects on markers of apoptosis. Forty adult Wistar albino rats were divided into four groups as control, α-LA, diabetic (DIA), and DIA+α-LA. For the induction of diabetes, the intraperitoneal injection of a dose of streptozotocin (STZ) (45 mg/kg) was used. α-LA (50 mg/kg) was applied to the groups of α-LA and DIA+α-LA for 14 days. At the end of the experiment, the brain cortex tissue and erythrocyte samples were taken from the rats. The levels of apoptosis, caspase 3, caspase 9, mitochondrial membrane potential, intracellular ROS, and lipid peroxidation were increased in the STZ group, although their levels were decreased in the DIA+α-LA group by the injection of α-LA. The STZ treatmentinduced decreases of cell viability, reduced glutathione, and glutathione peroxidase were increased in the brain and erythrocytes by the treatment of α-LA. In conclusion, diabetes acted a role in neuronal damage caused by increased ROS and apoptosis. We observed that α-LA induced a modulatory role on the apoptotic, oxidant, and antioxidant parameters in the brain and erythrocyte. The neuroprotective role of α-LA treatment may be explained by its modulating activity against increased oxidative stress and apoptosis.

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强抗氧化剂硫辛酸可降低糖尿病大鼠红细胞和脑细胞中stz诱导的氧化应激和细胞凋亡水平

糖尿病是世界上最重要的慢性健康问题之一，它引起氧化应激诱导的神经元损伤。在整个疾病过程中，它会导致严重的细胞损失和损伤。据推测，这一过程中氧化应激的增加增加了游离活性氧(ROS)和凋亡标志物，并导致糖尿病损伤。α-硫辛酸(α-LA)在ROS还原反应中具有直接的抗氧化作用，也是抗氧化系统中控制自由基和细胞凋亡的主要成分之一。为了了解α-LA在减少糖尿病诱导的氧化损伤中的作用，我们检测了大鼠大脑皮层和红细胞中ROS的产生及其对细胞凋亡标志物的影响。将40只成年Wistar白化大鼠分为对照组、α-LA组、糖尿病(DIA)组和DIA+α-LA组。为诱导糖尿病，采用腹腔注射链脲佐菌素(STZ) 1剂量(45 mg/kg)。α-LA组和DIA+α-LA组ig α-LA (50 mg/kg)， ig 14 d。实验结束时，取大鼠脑皮层组织和红细胞样本。注射α-LA后，DIA+α-LA组细胞凋亡、caspase 3、caspase 9、线粒体膜电位、细胞内ROS和脂质过氧化水平均降低，而STZ组细胞凋亡、caspase 3、caspase 9、细胞内ROS水平升高。STZ处理导致细胞活力降低，α-LA处理导致脑和红细胞中还原性谷胱甘肽和谷胱甘肽过氧化物酶升高。综上所述，糖尿病参与了由ROS和细胞凋亡增加引起的神经元损伤。我们观察到α-LA对脑和红细胞的凋亡、氧化和抗氧化参数具有调节作用。α-LA治疗的神经保护作用可能是通过其调节氧化应激和细胞凋亡的活性来解释的。

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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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)