Diabetes impairs hippocampal function via advanced glycation end product mediated new neuron generation in animals with diabetes-related depression.
Diabetes impairs hippocampal function via advanced glycation end product mediated new neuron generation in animals with diabetes-related depression.
复制标题
糖尿病通过晚期糖基化终末产物介导患有糖尿病相关抑郁症的动物的新神经元生成来损害海马功能。
DOI：
10.1093/toxsci/kfp126
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发表时间：
2009-09
期刊：
影响因子：
--
通讯作者：
Guo YI-jing
中科院分区：
文献类型：
--
作者：
Wang Shao-hua;Yuan Yang;Sun Zi-lin;Yang Bin-quan;Guo YI-jing
糖尿病引起的海马齿状神经发生减少及其抗抑郁药物的逆转意味着糖尿病相关抑郁和认知能力下降的潜在机制。在下面的文章中，根据体外研究进一步解释了晚期糖基化终产物（AGE）在患有抑郁症的糖尿病动物海马神经发生缺陷中的作用。使用链脲佐菌素（55 mg/kg，腹膜内注射）诱导动物患糖尿病，然后根据行为测试分析，将动物分为有抑郁样行为的动物和没有抑郁样行为的动物。 AGE 形成抑制剂氨基胍 (10 mg/kg) 再给药 4 周。使用溴脱氧尿苷标记和共聚焦激光显微镜监测增殖细胞、它们的存活和表型命运。使用流动注射测定来确定 AGE 肽的存在。患有糖尿病和抑郁症状的动物表现出海马神经发生减少和 AGE 肽血清水平升高，这两种情况都可以通过为期 4 周的氨基胍治疗方案（10 mg/kg，腹膜内注射）逆转，该方案抑制 AGE 形成；此外，抑郁行为也得到改善。这些发现提供了体内证据，表明糖尿病通过 AGE 介导的新神经元生成损害海马功能。这可能代表了一种导致糖尿病相关抑郁和认知能力下降的假定机制，并且为未来的研究提供了一种潜在的方法。
The diabetes-induced reduction of neurogenesis in hippocampal dentate and its reversal with antidepressant medications implies a potential mechanism for diabetes-related depression and cognitive decline. In the following article, the role of advanced glycation end products (AGEs) in hippocampal neurogenesis deficits in diabetic animals with depression has been further explained in the light of an in vitro study. Diabetes was induced in animals with the use of streptozotocin (55 mg/kg, i.p.), and the animals then divided into those with and those without depression-like behaviors as analyzed by behavioral tests. The AGE formation inhibitor aminoguanidine (10 mg/kg) was administrated for an additional 4 weeks. Proliferating cells, their survival, and their phenotype fate were monitored with bromodeoxyuridine labeling and confocal laser microscopy. The presence of AGE peptides was determined with the use of a flow injection assay. Animals with diabetes and depressive symptoms displayed a reduction in hippocampal neurogenesis and an elevated serum level of AGE peptides, both of which were reversed by a 4-week regimen of aminoguanidine (10 mg/kg, i.p.), which inhibits AGE formation; in addition, the depressive behaviors were improved. These findings provided in vivo evidence that diabetes impairs hippocampal function via the AGE-mediated generation of new neurons. This likely represents a putative mechanism that is responsible for diabetes-related depression and cognitive decline, and it suggests a potential approach for future research.
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DOI：
--
发表时间：
2003
期刊：
International journal of clinical pharmacology research
影响因子：
--
作者：
S. Yamagishi;M. Takeuchi;Y. Inagaki;Kei-ichiro Nakamura;T. Imaizumi
通讯作者：
S. Yamagishi;M. Takeuchi;Y. Inagaki;Kei-ichiro Nakamura;T. Imaizumi
DOI：
--
发表时间：
1997
期刊：
L'Encephale
影响因子：
--
作者：
J. Moreau
通讯作者：
J. Moreau
影响因子：
4.2
作者：
Messier, C
通讯作者：
Messier, C
影响因子：
8.2
作者：
N. Liu;Z. Sun;B. Liu
通讯作者：
N. Liu;Z. Sun;B. Liu
影响因子：
3.5
作者：
W. Zhang;Y.-F. Tan;J. Yue;M. Vranic;J. Wojtowicz
通讯作者：
W. Zhang;Y.-F. Tan;J. Yue;M. Vranic;J. Wojtowicz