中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (3): 451-456.doi: 10.4103/1673-5374.153695

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

1型糖尿病大鼠海马CA1区而非齿状回神经元最易受氧化应激损害

  

  • 收稿日期:2015-02-10 出版日期:2015-03-20 发布日期:2015-03-20
  • 基金资助:

    韩国政府国家研究基金(2010-0007712)

Neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes

Sang Gun Lee 1, Dae Young Yoo 2, Hyo Young Jung 2, Sung Min Nam 2, Jong Whi Kim 2, Jung Hoon Choi 3, Sun Shin Yi 4, Moo-Ho Won 5, Yeo Sung Yoon 2, In Koo Hwang 2, Seung Myung Moon 1   

  1. 1 Departments of Neurosurgery, Dongtan Sacred Heart Hospital, College of Medicine, Hallym University, Hwaseong 445-907, South Korea
    2 Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National
    University, Seoul 151-742, South Korea
    3 Department of Anatomy, College of Veterinary Medicine, Kangwon National University, Chuncheon 200-701, South Korea
    4 Department of Biomedical Laboratory Science, College of Medical Sciences, Soonchunhyang University, Asan 336-745, South Korea
    5 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea
  • Received:2015-02-10 Online:2015-03-20 Published:2015-03-20
  • Contact: Seung Myung Moon, M.D., Ph.D., nsmsm@chol.com or nsmsm@hallym.ac.kr.
  • Supported by:

    This work was supported by a National Research Foundation of Korea Grant funded by the Korean Government (MEST), Republic of Korea, No. 2010-0007712.

摘要:

为研究链脲佐菌素诱导的1型糖尿病大鼠海马抗氧化样蛋白1免疫反应,反映氧化应激诱导的蛋白修饰变化的蛋白羰基及脂质过氧化丙二醛形成的时空变化,实验给予成年大鼠腹腔注射链脲佐菌素75 mg/kg建立1型糖尿病模型,并于建模后2,3,4周进行检测。发现注射链脲佐菌素后3周糖尿病模型大鼠海马CA1区神经元抗氧化样蛋白1免疫反应明显降低,而齿状回区无此变化。同时发现模型大鼠海马蛋白羰基及脂质过氧化丙二醛水平明显升高。说明成年1型糖尿病大鼠海马CA1区神经元最易受氧化应激损伤,而非齿状回区神经元易受损伤。

关键词: 神经再生, 海马, 齿状回, 脂质过氧化, 糖尿病, 蛋白修饰, 丙二醛, 神经元

Abstract:

In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxidant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin (75 mg/kg) was intraperitoneally injected into adult rats to induce type 1 diabetes. The three experimental parameters were determined at 2, 3, 4 weeks after streptozotocin treatment. Fasting blood glucose levels significantly increased by 20.7–21.9 mM after streptozotocin treatment. The number of antioxidant-like protein-1 immunoreactive neurons significantly decreased in the hippocampal CA1 region, but not the dentate gyrus, 3 weeks after streptozotocin treatment compared to the control group. Malondialdehyde and protein carbonyl levels, which are modified by oxidative stress, significantly increased with a peak at 3 weeks after malondialdehyde treatment, and then decreased 4 weeks after malondialdehyde treatment. These results suggest that neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress 3 weeks after malondialdehyde treatment.

Key words: nerve regeneration, hippocampus, dentate gyrus, lipid peroxidation, type 1 diabetes, malondialdehyde, neurons, neural regeneration