n -乙酰半胱氨酸对实验性肥胖模型海马铁下垂的保护作用

Q4 Biochemistry, Genetics and Molecular Biology

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2023-09-29 DOI:10.37212/jcnos.1358141

Kiymet Kubra TÜFEKCİ, Musa TATAR

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引用次数: 0

摘要

铁死亡是一种非凋亡性细胞死亡，与铁超载、谷胱甘肽代谢失衡、氧化应激和脂质过氧化损伤等代谢途径密切相关。肥胖与这些失衡密切相关。在这项研究中，我们旨在探讨肥胖模型海马铁下垂的影响以及n -乙酰半胱氨酸(NAC)对铁下垂的潜在作用。采用高脂肪(60%)饮食模式建立肥胖模型，持续15周。NAC组和肥胖+NAC (ObNAC)组以150 mg/kg的剂量灌胃给予NAC，连续3周。采用免疫组织化学方法检测海马组织中谷胱甘肽过氧化物酶4 (GPX4)和胱氨酸转运蛋白溶质载体家族7-成员11 (SLC7A11)的表达水平。统计分析显示，Ob组海马组织中GPX4、SLC7A11的h -评分显著低于对照组、NAC组和ObNAC组(p

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Protective effect of N-acetylcysteine on hippocampal ferroptosis in an experimental obesity model

Ferroptosis is a non-apoptotic cell death closely related to a metabolic pathway involving iron overload, imbalanced glutathione metabolism, oxidative stress and lipid peroxidation damage. Obesity is closely associated with these imbalances. In this study, we aimed to investigate the effect of hippocampal ferroptosis in an obesity model and the potential role of N-acetylcysteine (NAC) against ferroptosis. A high-fat (60%) dietary pattern was used to establish an obesity model for 15 weeks. NAC was administered to NAC and Obese+NAC (ObNAC) groups by oral gavage at a dose of 150 mg/kg for 3 weeks. Glutathione peroxidase 4 (GPX4) and the cystine transporter solute carrier family 7- member 11 (SLC7A11) expression levels were investigated immunohistochemically to detect ferroptosis in hippocampal tissues. In the statistical analysis, H-scores of GPX4 and SLC7A11 in the hippocampus sections of the Ob group were significantly lower than in the control, NAC and ObNAC groups (p

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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)