首页> 外文期刊>Journal of toxicology and environmental health, Part A >Protective effects of testosterone on cognitive dysfunction in Alzheimer's disease model rats induced by oligomeric beta amyloid peptide 1-42
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Protective effects of testosterone on cognitive dysfunction in Alzheimer's disease model rats induced by oligomeric beta amyloid peptide 1-42

机译:睾酮对阿尔茨海默病模型大鼠抗原蛋白蛋白肽1-42诱导的阿尔茨海默病模型大鼠认知功能障碍的保护作用

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摘要

Cognitive dysfunction is known to be influenced by circulating sex steroidal hormones. The aim of this study was to examine the protective effect and possible protective mechanism of testosterone (T) on cognitive performance in male rats induced by intrahippocampal injections of beta amyloid 1-42 oligomers (A1-42). Treatment with T as evidenced by the Morris water maze (MWM) test significantly shortened escape latency and reduced path length to reach the platform compared to the control (C). During probe trials, the T group displayed a significantly greater percent of time in the target quadrant and improved the number of platform crossings compared with C, flutamide (F), an antiandrogen, and a combined F and T group. Flutamide markedly inhibited the influence of T on cognitive performance. Following Nissl staining, the number of intact pyramidal cells was significantly elevated in the T group, and the effect of T was blocked by F. Immunohistochemisty and Western blot analysis showed that the protein expression level of A 1-42 was markedly decreased and expression levels of synaptophysin (SYN) significantly increased with T, while F inhibited all T-mediated effects. Our data suggest that the influence of T on cognitive performance was mediated via androgen receptors (AR) to remove beta amyloid, which leads to enhanced synaptic plasticity.
机译:已知认知功能障碍受循环性甾体激素的影响。本研究的目的是检测睾酮(T)对β淀粉样蛋白1-42低聚物(A1-42)的血液捕获剂杂交诱导的雄性大鼠认知性能的保护作用和可能的保护机制。与莫里斯水迷宫(MWM)测试证明的T治疗显着缩短了逃逸延迟和降低的路径长度,以与控制(C)相比到达平台。在探测试验期间,T组在靶象限中显示出明显更大的时间百分比,与C,氟氨酰胺(F),抗衰老糖尿病和F和T组相比改善了平台交叉的数量。氟氨基显着抑制T对认知性能的影响。在NISSL染色之后,在T组中,完整的金字塔细胞的数量显着升高,F的效果由F.免疫组化和Western印迹分析显示1-42的蛋白表达水平显着降低和表达水平突触甘油(SYN)与T显着增加,而F抑制所有T介导的效果。我们的数据表明,T对认知性能的影响是通过雄激素受体(AR)介导的,以除去β淀粉样蛋白,这导致突触塑性增强。

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