中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (2): 232-241.doi: 10.4103/1673-5374.265543

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

硫化氢对氧化应激诱导神经退行性疾病的保护

  

  • 出版日期:2020-02-15 发布日期:2020-05-23
  • 基金资助:

    韩国科学,信息通信技术和未来规划部资助(2018R1A2B6001123;2018R1D1A1B07040282)

Protective effect of hydrogen sulfide on oxidative stress-induced neurodegenerative diseases

Rubaiya Tabassum1, 2, Na Young Jeong1, 2 Junyang Jung3   

  1. 1 Department of Anatomy and Cell Biology, College of Medicine, Dong-A University, Seo-gu, Busan, Korea
    2 Department of Medicine, Graduate School, Dong-A University, Seo-gu, Busan, Korea
    3 Department of Anatomy and Neurobiology, College of Medicine, Kyung Hee University, Dongdaemun-gu, Seoul, Korea
  • Online:2020-02-15 Published:2020-05-23
  • Contact: Na Young Jeong, MD, PhD,jnyjjy@dau.ac.kr;Junyang Jung, MD, PhD,jjung@khu.ac.kr.
  • Supported by:
    This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT and Future Planning, No. 2018R1A2B6001123 (to NYJ), No. 2018R1D1A1B07040282 (to JJ).

摘要:

硫化氢具有广泛的抗氧化应激生物效应,平衡的氧化应激对于维持生物系统中的细胞功能至关重要。当正常的氧化还原平衡被扰乱时,脱氧核糖核酸、脂质和蛋白质分子在病理状态下被氧化,导致糖尿病周围神经病变的发生,神经元细胞中的葡萄糖代谢受到干扰。高血糖水平导致与阿尔茨海默病、帕金森病和肌萎缩侧索硬化症等合并症相关的认知功能障碍。氧化应激在抑制脑功能所必需的胰岛素信号传导中起作用;硫化氢显示出抗氧化应激作用,其中胱硫醚β合成酶、胱硫醚γ裂解酶和3-巯基丙酮酸硫转移酶是硫化氢的内源性来源。综述将探讨糖尿病周围神经病变和其他神经退行性疾病在氧化应激条件下的发病机制,以及硫化氢发挥的抗氧化作用。

orcid: 0000-0002-1738-1335 (Rubaiya Tabassum) 

         0000-0003-2130-4719 (Na Young Jeong) 

         0000-0003-3946-5406 (Junyang Jung)

关键词: 硫化氢, 氧化应激, 抗氧化剂, 活性氧, DNA氧化, 线粒体功能障碍, 糖尿病周围神经病变, 阿尔茨海默氏病, 帕金森病, 肌萎缩侧索硬化

Abstract: Hydrogen sulfide is an antioxidant molecule that has a wide range of biological effects against oxidative stress. Balanced oxidative stress is also vital for maintaining cellular function in biological system, where reactive oxygen species are the main source of oxidative stress. When the normal redox balance is disturbed, deoxyribonucleic acid, lipid, and protein molecules are oxidized under pathological conditions, like diabetes mellitus that leads to diabetic peripheral neuropathy. In diabetes mellitus-induced diabetic peripheral neuropathy, due to hyperglycemia, pancreatic beta cell (β cell) shows resistance to insulin secretion. As a consequence, glucose metabolism is disturbed in neuronal cells which are distracted from providing proper cell signaling pathway. Not only diabetic peripheral neuropathy but also other central damages occur in brain neuropathy. Neurological studies regarding type 1 diabetes mellitus patients with Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis have shown changes in the central nervous system because high blood glucose levels (HbA1c) appeared with poor cognitive function. Oxidative stress plays a role in inhibiting insulin signaling that is necessary for brain function. Hydrogen sulfide exhibits antioxidant effects against oxidative stress, where cystathionine β synthase, cystathionine γ lyase, and 3-mercaptopyruvate sulfurtransferase are the endogenous sources of hydrogen sulfide. This review is to explore the pathogenesis of diabetes mellitus-induced diabetic peripheral neuropathy and other neurological comorbid disorders under the oxidative stress condition and the anti-oxidative effects of hydrogen sulfide.

Key words: Alzheimer’s disease, amyotrophic lateral sclerosis, antioxidant, diabetic peripheral neuropathy, DNA oxidation, hydrogen sulfide, mitochondrial dysfunction, oxidative stress, Parkinson’s disease, reactive oxygen species