N-乙酰半胱氨酸通过抑制半胱天冬酶-3减轻氧化应激并保护大鼠海马免受辐射诱导的细胞凋亡。

N-acetylcysteine relieves oxidative stress and protects hippocampus of rat from radiation-induced apoptosis by inhibiting caspase-3.

作者信息

Li Jianguo, Meng Zhuangzhi, Zhang Guowei, Xing Yonghua, Feng Li, Fan Saijun, Fan Feiyue, Buren Batu, Liu Qiang

机构信息

Laboratory of Biomedicine & Department of Hemopathic Tumor of Mongolian Medicine, The Affiliated Hospital of Inner Mongolia University for the Nationalities, Neimenggu Tongliao, PR China; Tianjin Key Lab of Molecular Nuclear Medicine, Institute of Radiation Medicine of Chinese Academy of Medical Science and Peking Union Medical College, Tianjin, PR China; Department of Human Anatomy, The Medical School of Inner Mongolia University for the Nationalities, Neimenggu Tongliao, PR China.

Department of Human Anatomy, The Medical School of Inner Mongolia University for the Nationalities, Neimenggu Tongliao, PR China.

出版信息

Biomed Pharmacother. 2015 Mar;70:1-6. doi: 10.1016/j.biopha.2014.12.029. Epub 2014 Dec 24.

Abstract

It has been recognized that radiation-induced effects remain a significant risk. An accumulation of reactive oxygen species (ROS) is considered to be one factor that contributes to neurodegenerative changes. The aim of our study was to investigate the potential radioprotective effects of NAC. Male Sprague-Dawley rats underwent radiation. Irradiation was performed at room temperature with a 4-Gy dose of radiation. A dose of N-acetylcysteine (NAC) was performed 15 min prior to irradiation intraperitoneally. The methods of immunohistochemistry, TUNEL staining, Nissl staining, qRT-PCR, analysis of reactive oxygen species and Western blot were performed. In conclusion, our results demonstrate that NAC inhibits apoptosis induced by irradiation via the inhibition of caspase-3. We demonstrated a decrease in caspase-3 mRNA that was present at 24h of NAC treatment. Such mRNA decrease was accompanied by a decrease of protein. In the present study, NAC effectively antagonized oxidation induced by irradiation. These results provide evidence that the neural protective effect and the antioxidant effect of NAC contribute to metabolic activity.

摘要

人们已经认识到,辐射诱导的效应仍然是一个重大风险。活性氧(ROS)的积累被认为是导致神经退行性变化的一个因素。我们研究的目的是调查N-乙酰半胱氨酸(NAC)的潜在辐射防护作用。雄性Sprague-Dawley大鼠接受辐射。在室温下以4 Gy的辐射剂量进行照射。在照射前15分钟腹腔注射一剂N-乙酰半胱氨酸(NAC)。采用免疫组织化学、TUNEL染色、尼氏染色、qRT-PCR、活性氧分析和蛋白质印迹法。总之,我们的结果表明,NAC通过抑制caspase-3来抑制辐射诱导的细胞凋亡。我们证明在NAC处理24小时时,caspase-3 mRNA减少。这种mRNA的减少伴随着蛋白质的减少。在本研究中,NAC有效地拮抗了辐射诱导的氧化。这些结果提供了证据,表明NAC的神经保护作用和抗氧化作用有助于代谢活性。

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