• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

肌醇可使链脲佐菌素诱导的糖尿病模型中血脑屏障降低的钠通透性恢复正常。

Myo-inositol normalizes decreased sodium permeability of the blood-brain barrier in streptozotocin diabetes.

作者信息

Knudsen G M, Jakobsen J, Barry D I, Compton A M, Tomlinson D R

机构信息

Department of Neurology, Rigshospitalet, Copenhagen, Denmark.

出版信息

Neuroscience. 1989;29(3):773-7. doi: 10.1016/0306-4522(89)90148-6.

DOI:10.1016/0306-4522(89)90148-6
PMID:2525678
Abstract

The effect of a dietary supplement of an aldose reductase inhibitor (ponalrestat) or of myo-inositol on sodium transport into the rat brain and on concentrations of saccharide and polyols in cortical brain tissue and sciatic nerve was investigated in control rats and in streptozotocin-diabetic rats after a diabetes duration of 2 weeks. In untreated diabetes, the neocortical blood-brain barrier permeability for sodium decreased by 28% (3.4 +/- 0.4 vs 4.7 +/- 1.6 x 10(-5) ml/s g, mean +/- SD) as compared to controls. Levels of glucose, sorbitol and fructose increased in brain as well as in nerve tissues, whereas myo-inositol depletion was not demonstrable. Ponalrestat treatment of diabetic animals had no effect upon the decreased neocortical blood-brain barrier permeability to sodium (3.5 +/- 0.9 vs 4.7 +/- 1.1 x 10(-5) ml/s g) despite normalization of brain and nerve content of sorbitol and fructose. Myo-inositol supplementation of diabetic rats normalized sodium passage into the brain (4.2 +/- 1.1 vs 4.4 +/- 0.5 x 10(-5) ml/s g). Brain concentrations of monosaccharides and polyols were normalized as compared to the myo-inositol treated control group and nerve concentrations of glucose, sorbitol, and fructose were significantly increased. Myo-inositol treatment leads to a normalization of blood-brain barrier permeability; it is suggested that myo-inositol exerts a restituting effect upon Na+/K+-ATPase activity of the cerebral endothelial cells.

摘要

在对照大鼠和糖尿病病程为2周的链脲佐菌素诱导的糖尿病大鼠中,研究了膳食补充醛糖还原酶抑制剂(泊那司他)或肌醇对钠转运入大鼠脑内以及对大脑皮质组织和坐骨神经中糖类和多元醇浓度的影响。在未经治疗的糖尿病大鼠中,与对照组相比,新皮质血脑屏障对钠的通透性降低了28%(3.4±0.4对4.7±1.6×10⁻⁵ ml/s g,平均值±标准差)。脑和神经组织中的葡萄糖、山梨醇和果糖水平升高,而肌醇耗竭未得到证实。对糖尿病动物进行泊那司他治疗,尽管脑和神经中山梨醇和果糖含量恢复正常,但对新皮质血脑屏障对钠通透性降低并无影响(3.5±0.9对4.7±1.1×10⁻⁵ ml/s g)。给糖尿病大鼠补充肌醇可使钠进入脑内的过程恢复正常(4.2±1.1对4.4±0.5×10⁻⁵ ml/s g)。与肌醇治疗的对照组相比,脑中的单糖和多元醇浓度恢复正常,神经中葡萄糖、山梨醇和果糖的浓度显著升高。肌醇治疗可使血脑屏障通透性恢复正常;提示肌醇对脑内皮细胞的Na⁺/K⁺-ATP酶活性具有恢复作用。

相似文献

1
Myo-inositol normalizes decreased sodium permeability of the blood-brain barrier in streptozotocin diabetes.肌醇可使链脲佐菌素诱导的糖尿病模型中血脑屏障降低的钠通透性恢复正常。
Neuroscience. 1989;29(3):773-7. doi: 10.1016/0306-4522(89)90148-6.
2
An aldose reductase inhibitor but not myo-inositol blocks enhanced polyphosphoinositide turnover in peripheral nerve from diabetic rats.一种醛糖还原酶抑制剂而非肌醇可阻断糖尿病大鼠外周神经中增强的多磷酸肌醇代谢。
Metabolism. 1996 Mar;45(3):320-7. doi: 10.1016/s0026-0495(96)90285-1.
3
Normalization of Na(+)-K(+)-ATPase activity in isolated membrane fraction from sciatic nerves of streptozocin-induced diabetic rats by dietary myo-inositol supplementation in vivo or protein kinase C agonists in vitro.通过体内补充膳食肌醇或体外使用蛋白激酶C激动剂,使链脲佐菌素诱导的糖尿病大鼠坐骨神经分离膜组分中的Na(+)-K(+)-ATP酶活性恢复正常。
Diabetes. 1991 May;40(5):558-67. doi: 10.2337/diab.40.5.558.
4
Slow component-a of axonal transport, nerve myo-inositol, and aldose reductase inhibition in streptozocin-diabetic rats.链脲佐菌素诱导的糖尿病大鼠轴突运输的慢成分-a、神经肌醇及醛糖还原酶抑制作用
Diabetes. 1986 Apr;35(4):398-402. doi: 10.2337/diab.35.4.398.
5
Increased nerve polyol levels in experimental diabetes and their reversal by Sorbinil.实验性糖尿病中神经多元醇水平升高及索比尼尔对其的逆转作用。
Br J Exp Pathol. 1988 Oct;69(5):697-702.
6
Impaired rat sciatic nerve sodium-potassium adenosine triphosphatase in acute streptozocin diabetes and its correction by dietary myo-inositol supplementation.急性链脲佐菌素诱导糖尿病大鼠坐骨神经钠钾腺苷三磷酸酶受损及其通过膳食补充肌醇的纠正作用。
J Clin Invest. 1983 Sep;72(3):1058-63. doi: 10.1172/JCI111030.
7
Transport of myo-inositol into endoneurial preparations of sciatic nerve from normal and streptozotocin-diabetic rats.肌醇向正常大鼠和链脲佐菌素诱导的糖尿病大鼠坐骨神经神经内膜制剂中的转运。
Biochem J. 1983 Mar 15;210(3):775-81. doi: 10.1042/bj2100775.
8
Relation of Na+, K(+)-ATPase to delayed motor nerve conduction velocity: effect of aldose reductase inhibitor, ADN-138, on Na+, K(+)-ATPase activity.钠钾ATP酶与运动神经传导速度延迟的关系:醛糖还原酶抑制剂ADN - 138对钠钾ATP酶活性的影响。
Metabolism. 1990 Jun;39(6):563-7. doi: 10.1016/0026-0495(90)90019-9.
9
Effect of myo-inositol on renal Na-K-ATPase in experimental diabetes.肌醇对实验性糖尿病大鼠肾钠钾ATP酶的影响
Metabolism. 1990 Oct;39(10):1026-32. doi: 10.1016/0026-0495(90)90161-5.
10
Reversal of deficits in axonal transport and nerve conduction velocity by treatment of streptozotocin-diabetic rats with myo-inositol.用肌醇治疗链脲佐菌素诱导的糖尿病大鼠可逆转轴突运输和神经传导速度的缺陷。
Exp Neurol. 1985 Aug;89(2):420-7. doi: 10.1016/0014-4886(85)90101-3.

引用本文的文献

1
ASK1 modulates the expression of microRNA Let7A in microglia under high glucose in vitro condition.在体外高糖条件下,ASK1调节小胶质细胞中微小RNA Let7A的表达。
Front Cell Neurosci. 2015 May 20;9:198. doi: 10.3389/fncel.2015.00198. eCollection 2015.
2
High glucose stimulates TNFα and MCP-1 expression in rat microglia via ROS and NF-κB pathways.高葡萄糖通过 ROS 和 NF-κB 通路刺激大鼠小胶质细胞中 TNFα 和 MCP-1 的表达。
Acta Pharmacol Sin. 2011 Feb;32(2):188-93. doi: 10.1038/aps.2010.174.
3
Cerebral function in diabetes mellitus.
糖尿病中的脑功能
Diabetologia. 1994 Jul;37(7):643-50. doi: 10.1007/BF00417687.