中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (8): 864-871.doi: 10.4103/1673-5374.131602

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

甲状腺素保护自然衰老动物海马区胆碱能神经元的功能

  

  • 收稿日期:2014-01-09 出版日期:2014-04-25 发布日期:2014-04-25
  • 基金资助:

    中国国家自然科学基金项目(81273416),中央高校基本科研业务费专项资金资助(XDJK2013A030)

The synthetic thyroid hormone, levothyroxine, protects cholinergic neurons in the hippocampus of naturally aged mice

Ailing Fu, Rumei Zhou, Xingran Xu   

  • Received:2014-01-09 Online:2014-04-25 Published:2014-04-25
  • Contact: Ailing Fu, School of Pharmaceutical Sciences, Southwest University, Tiansheng Road, Beibei District, Chongqing 400716, China, Fuailing1008@hotmail.com.
  • Supported by:

    This work is supported by the National Natural Science Foundation of China, No. 81273416, and Fundamental Research Funds for the Central Universities, No. XDJK2013A030.

摘要:

甲状腺激素包括三碘甲状腺氨酸和甲状腺素,在哺乳动物的认知功能中起重要作用。然而,至今少见使用甲状腺素改善自然衰老动物存活率和神经元功能的研究。在此,我们设计了给予老年CD-1小鼠腹腔注射小剂量左旋甲状腺素3个月后,检测海马神经元出现细胞骨架重排,突触功能明显增加,血清激素水平增加,且海马胆碱乙酰化转移酶、神经递质乙酰胆碱水平及氧酶超氧化物歧化酶活性增加,小鼠存活率从60%提高到93%,老年小鼠的认知能力明显改善的结果。意义在于从老年动物补充少量左旋甲状腺素可改善认知区神经元功能的角度可考虑其转化医学价值。

关键词: 神经再生, 脑损伤, 海马, 胆碱能神经元, 左旋甲状腺素, 衰老, 学习记忆, 存活率, 认知障碍, NSFC grant

Abstract:

The thyroid hormones, triiodothyronine and thyroxine, play important roles in cognitive function during the mammalian lifespan. However, thyroid hormones have not yet been used as a therapeutic agent for normal age-related cognitive deficits. In this study, CD-1 mice (aged 24 months) were intraperitoneally injected with levothyroxine (L-T4; 1.6 μg/kg per day) for 3 consecutive months. Our findings revealed a significant improvement in hippocampal cytoskeletal rearrangement of actin and an increase in serum hormone levels of L-T4-treated aged mice. Furthermore, the survival rate of these mice was dramatically increased from 60% to 93.3%. The Morris water maze task indicated that L-T4 restored impaired spatial memory in aged mice. Furthermore, level of choline acetyltransferase, acetylcholine, and superoxide dismutase were increased in these mice, thus suggesting that a possible mechanism by which L-T4 reversed cognitive impairment was caused by increased activity of these markers. Overall, supplement of low-dosage L-T4 may be a potential therapeutic strategy for normal age-related cognitive deficits.

Key words: nerve regeneration, brain injury, hippocampus, cholinergic neurons, levothyroxine, aging, learning and memory, survival rate, cognitive disorder, NSFC grant, neural regeneration

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