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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db~-/db~- mouse, a type 2 diabetes model
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Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db~-/db~- mouse, a type 2 diabetes model

机译：辅酶Q10可预防db〜-/ db〜-小鼠（一种2型糖尿病模型）的周围神经病变并减轻其神经元损失

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Department of Molecular Medicine and Surgery, Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska University Hospital, 171 76 Stockholm, Sweden,School of Life Science and Technology, Harbin Institute of Technology, 150001 Harbin, China,Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden,Department of Dental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden;School of Life Science and Technology, Harbin Institute of Technology, 150001 Harbin, China,Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden,Department of Dental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden;Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;Department of Molecular Medicine and Surgery, Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska University Hospital, 171 76 Stockholm, Sweden;Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;School of Life Science and Technology, Harbin Institute of Technology, 150001 Harbin, China,Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;Department of Clinical Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;Department of Dental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden;Department of Molecular Medicine and Surgery, Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska University Hospital, 171 76 Stockholm, Sweden;Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060-8638, Japan;Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;Department of Molecular Medicine and Surgery, Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska University Hospital, 171 76 Stockholm, Sweden;Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;%Diabetic peripheral neuropathy (DPN) is the most common complication in both type 1 and type 2 diabetes. Here we studied some phenotypic features of a well-established animal model of type 2 diabetes, the leptin receptor-deficient db~/db~ mouse, and also the effect of long-term (6 mo) treatment with coenzyme Q10 (CoQ10), an endogenous antioxidant. Diabetic mice at 8 mo of age exhibited loss of sensation, hypoalgesia (an increase in mechanical threshold), and decreases in mechanical hyperalgesia, cold allodynia, and sciatic nerve conduction velocity. All these changes were virtually completely absent after the 6-mo, daily CoQ10 treatment in db~-/db~- mice when started at 7 wk of age. There was a 33% neuronal loss in the lumbar 5 dorsal root ganglia (DRGs) of the db~-/db~- mouse versus controls at 8 mo of age, which was significantly attenuated by CoQ10. There was no difference in neuron number in 5/6-wk-old mice between diabetic and control mice. We observed a strong down-regulation of phospholipase C (PLC) β3 in the DRGs of diabetic mice at 8 mo of age, a key molecule in pain signaling, and this effect was also blocked by the 6-mo CoQ10 treatment. Many of the phenotypic, neurochemical regulations encountered in lumbar DRGs in standard models of peripheral nerve injury were not observed in diabetic mice at 8 mo of age. These results suggest that reactive oxygen species and reduced PLCβ3 expression may contribute to the sensory deficits in the late-stage diabetic db/db~ mouse, and that early long-term administration of the antioxidant CoQ10 may represent a promising therapeutic strategy for type 2 diabetes neuropathy.
机译：卡罗林斯卡大学医院Rolf Luft糖尿病与内分泌学研究中心分子医学与外科系，斯德哥尔摩，171 76，瑞典，哈尔滨工业大学生命科学与技术学院，150001哈尔滨，中国，卡罗林斯卡学院神经科学系， 171 77瑞典斯德哥尔摩，卡罗林斯卡学院牙科医学系，171 77斯德哥尔摩，瑞典；哈尔滨工业大学生命科学与技术学院，150001哈尔滨，中国卡罗林斯卡学院神经科学系，171 77斯德哥尔摩，瑞典，瑞典卡罗林斯卡学院牙科医学系，斯德哥尔摩171 77;瑞典卡罗林斯卡学院神经科学系，瑞典171 77;瑞典斯德哥尔摩卡罗林斯卡学院神经科学系，171 77斯德哥尔摩;罗尔夫·卢夫研究中心分子医学与外科瑞典卡罗林斯卡大学医院糖尿病和内分泌学中心，171 76瑞典斯德哥尔摩;卡罗市神经科学系瑞典林斯卡学院171 77；瑞典哈尔滨工业大学生命科学与技术学院，哈尔滨150001瑞典卡罗林斯卡学院神经科学系，瑞典171 77斯德哥尔摩；瑞典卡罗林斯卡学院神经科学科171斯德哥尔摩瑞典;卡罗林斯卡学院牙科医学系，瑞典171 77;瑞典卡罗林斯卡大学医院Rolf Luft糖尿病与内分泌学研究中心分子医学与外科系，瑞典171 76;北海道大学学院解剖学系日本，札幌060-8638；瑞典卡罗林斯卡学院神经科学系，瑞典171 77；瑞典卡罗林斯卡大学医院Rolf Luft糖尿病和内分泌学研究中心分子医学与外科系，瑞典斯德哥尔摩171 76；瑞典卡罗林斯卡研究所神经科学学院，171 77斯德哥尔摩，瑞典；糖尿病周围神经病（DPN）是最常见的并发症1型和2型糖尿病中的阳离子。在这里，我们研究了成熟的2型糖尿病动物模型，瘦素受体缺陷型db〜/ db〜小鼠的一些表型特征，以及辅酶Q10（CoQ10）长期（6 mo）治疗的效果，内源性抗氧化剂。 8个月大的糖尿病小鼠表现出感觉丧失，痛觉过敏（机械阈值增加），机械痛觉过敏，冷异常性疼痛和坐骨神经传导速度降低。从7周龄开始，在db〜-/ db〜-小鼠中每天进行6个月的CoQ10每日治疗后，实际上几乎完全没有这些变化。 db〜-/ db〜-小鼠的腰5背根神经节（DRG）与对照组相比在8 mo时有33％的神经元丢失，这被CoQ10明显减轻。在5 / 6-wk龄小鼠中，糖尿病小鼠和对照组小鼠的神经元数量没有差异。我们在8个月大的糖尿病小鼠的DRG中观察到了磷酸酶C（PLC）β3的强烈下调，这是疼痛信号中的关键分子，而6个月CoQ10处理也阻止了这种作用。在8周龄的糖尿病小鼠中，未观察到在周围神经损伤的标准模型中腰部DRG遇到的许多表型，神经化学调控。这些结果表明，活性氧和降低的PLCβ3表达可能会导致晚期db / db〜小鼠的感觉缺陷，并且早期长期服用抗氧化剂CoQ10可能代表2型糖尿病的有希望的治疗策略。神经病。

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  • 作者

    Tie-Jun Sten Shi; Ming-Dong Zhang; Hugo Zeberg; Johanna Nilsson; Jacob Gruenler; Su-Xing Liu; Qiong Xiang; Jonas Persson; Kaj J. Fried; Sergiu Bogdan Catrina; Masahiko Watanabe; Peter Arhem; Kerstin Brismar; Tomas G. M. Hoekfelt;

  • 作者单位

    Department of Molecular Medicine and Surgery, Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska University Hospital, 171 76 Stockholm, Sweden,School of Life Science and Technology, Harbin Institute of Technology, 150001 Harbin, China,Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden,Department of Dental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden;

    School of Life Science and Technology, Harbin Institute of Technology, 150001 Harbin, China,Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden,Department of Dental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden;

    Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;

    Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;

    Department of Molecular Medicine and Surgery, Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska University Hospital, 171 76 Stockholm, Sweden;

    Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;

    School of Life Science and Technology, Harbin Institute of Technology, 150001 Harbin, China,Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;

    Department of Clinical Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;

    Department of Dental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden;

    Department of Molecular Medicine and Surgery, Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska University Hospital, 171 76 Stockholm, Sweden;

    Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060-8638, Japan;

    Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;

    Department of Molecular Medicine and Surgery, Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska University Hospital, 171 76 Stockholm, Sweden;

    Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    neurodegeneration; neuropeptide; electrophysiology;

    机译：神经变性神经肽电生理;

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