中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (5): 555-560.doi: 10.4103/1673-5374.130080

• 原著:脑损伤修复保护与再生 • 上一篇    

丙烯酰胺暴露可导致血脑脊液屏障功能失调

  

  • 收稿日期:2014-01-27 出版日期:2014-03-12 发布日期:2014-03-12

Acrylamide exposure impairs blood-cerebrospinal fluid barrier function

Xue Yao 1, Licheng Yan 1, Lin Yao 2, Weijun Guan 3, Fanxu Zeng 1, Fuyuan Cao 2, Yanshu Zhang 1   

  1. 1 College of Public Health, Hebei United University, Tangshan, Hebei Province, China
    2 Experimental Animal Center, Hebei United University, Tangshan, Hebei Province, China
    3 Key Laboratory of Hebei Health and Safety on Coal Industry, Hebei United University, Tangshan, Hebei Province, China
  • Received:2014-01-27 Online:2014-03-12 Published:2014-03-12
  • Contact: Yanshu Zhang, Ph.D., College of Public Health, Hebei United University, Tangshan 063000, Hebei Province, China, Yanshu_zhang@163.com.
  • Supported by:

    This study was supported by State Key Development Program for Basic Research of China, No. 2012CB525002 and the National Natural Science Foundation of China, No. 30771823.

摘要:

已有一些研究证实,慢性丙烯酰胺暴露导致中枢及周围神经病变。实验对大鼠进行丙烯酰胺染毒,在染毒后第7,14,21和28天,检测染毒大鼠血脑脊液屏障通透性、分泌转甲状腺素蛋白和转运瘦素的功能。结果显示,染毒第7天时脑脊液中甲状腺素蛋白含量开始下降,染毒第14天时脑脊液中荧光素钠的含量上升,染毒第28天时脑脊液/血清白蛋白比值增加,染毒第21,28天时脑脊液中伊文思蓝含量增加,同时脑脊液/血清中瘦素的比值下降。这些变化证实,丙烯酰胺暴露损伤了血脑脊液屏障的通透及分泌和转运功能,导致血脑脊液屏障的保护性功能失调,这可能是丙烯酰胺致神经毒性的作用机制之一。

关键词: 神经再生, 脑损伤, 丙烯酰胺, 血-脑脊液屏障, 紧密连接, 渗透, 甲状腺素, 瘦素, 脑脊液/血清白蛋白比值, 脑脊液

Abstract:

Previous studies show that chronic acrylamide exposure leads to central and peripheral neuropathy. However, the underlying mechanisms remained unclear. In this study, we examined the permeability of the blood-cerebrospinal fluid barrier, and its ability to secrete transthyretin and transport leptin of rats exposed to acrylamide for 7, 14, 21 or 28 days. Transthyretin levels in cerebrospinal fluid began to decline on day 7 after acrylamide exposure. The sodium fluorescein level in cerebrospinal fluid was increased on day 14 after exposure. Evans blue concentration in cerebrospinal fluid was increased and the cerebrospinal fluid/serum leptin ratio was decreased on days 21 and 28 after exposure. In comparison, the cerebrospinal fluid/serum albumin ratio was increased on day 28 after exposure. Our findings show that acrylamide exposure damages the blood-cerebrospinal fluid barrier and impairs secretory and transport functions. These changes may underlie acrylamide-induced neurotoxicity.

Key words: nerve regeneration, brain injury, acrylamide, blood-cerebrospinal fluid barrier, tight junction, permeability, thyroid hormone, leptin, cerebrospinal fluid/serum albumin ratio, cerebrospinal fluid, NSFC grant, neural regeneration