首页> 外文期刊>International Journal of Neuroscience >NMDA receptor subunits 2A and 2B decrease and lipid peroxidation increase in the hippocampus of streptozotocin-diabetic rats: effects of insulin and gliclazide treatments.
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NMDA receptor subunits 2A and 2B decrease and lipid peroxidation increase in the hippocampus of streptozotocin-diabetic rats: effects of insulin and gliclazide treatments.

机译:链脲佐菌素-糖尿病大鼠海马中NMDA受体亚基2A和2B减少,脂质过氧化增加:胰岛素和格列齐特治疗的作用。

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摘要

Recent studies indicate that diabetes mellitus changes N-methyl-D-aspartate (NMDA) receptor subunit composition and impairs cognitive functions. It also has been known that diabetes mellitus causes lipid peroxidation. This study examined the effects of streptozotocin-diabetes and insulin or gliclazide treatment on the hippocampal NMDA receptor subunit 2A and 2B (NR2A and NR2B) concentrations. In addition, malondial dehyde (MDA) levels were measured as a marker for lipid peroxidation. Eight weeks after the induction of diabetes MDA, levels were increased, and NR2A and NR2B concentrations were reduced. Insulin and gliclazide treatment partially prevented the reduction of NR2A and NR2B expression and prevented the elevation of MDA levels. There was no significant difference between the effects of insulin and gliclazide. The results suggest that the elevation of lipid peroxidation can be the primary biochemical disturbances in diabetes progression, and that changes in NMDA receptor subunit compositions canbe involved in cognitive decline in diabetes.
机译:最近的研究表明,糖尿病会改变N-甲基-D-天冬氨酸(NMDA)受体亚基的组成并损害认知功能。还已知糖尿病引起脂质过氧化。这项研究检查了链脲佐菌素-糖尿病和胰岛素或格列齐特治疗对海马NMDA受体亚基2A和2B(NR2A和NR2B)浓度的影响。另外,测量丙二醛(MDA)水平作为脂质过氧化的标志物。诱发糖尿病MDA后八周,其水平升高,NR2A和NR2B浓度降低。胰岛素和格列齐特治疗部分阻止了NR2A和NR2B表达的降低,并阻止了MDA水平的升高。胰岛素和格列齐特的作用之间无显着差异。结果表明,脂质过氧化作用的升高可能是糖尿病进展的主要生化障碍,而NMDA受体亚基组成的变化可能与糖尿病的认知能力下降有关。

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