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首页> 外文期刊>Psychiatry and Clinical Psychopharmacology >Effects of agmatine on cognitive functions during vascular dementia in biological aging through eNOS and BDNF expression
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Effects of agmatine on cognitive functions during vascular dementia in biological aging through eNOS and BDNF expression

机译：胍丁胺通过eNOS和BDNF表达对生物衰老过程中血管性痴呆认知功能的影响

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Objective: Biological aging has been recognized to cause impairment of memory and the development of vascular dementia. Based on our previous work, agmatine has been shown to have a beneficial effect and might have therapeutic potential on cognitive functions, including learning and memory. The aim of the present study was to examine the possible effect of agmatine on biological aging-induced vascular endothelial dysfunction and associated dementia in rats.Methods: We used three different age groups (4-month-olds, 18-month-olds and 24-month-olds; n ?=?12 in each group) of control and agmatine-treated rats. Control animals received physiological saline for 8 weeks. Agmatine sulfate (40?mg/kg, twice daily) was given to the agmatine groups orally for 8 weeks. Herein, we investigated the effects of agmatine on systolic blood pressure (SBP), nitric oxide (NO)-mediated endothelium-dependent and -independent vasorelaxant responses in thoracic aorta, cognitive performance (passive avoidance test; PAT, and Morris water maze test; MWMT), endothelial nitric oxide synthase (eNOS) expression and both hippocampal and amygdaloid brain-derived neurotrophic factor (BDNF) expression in aged rats.Results: We found cognitive decline, endothelial dysfunction and reduced eNOS and BDNF expression in aged rats. All these changes may result from aging-induced vascular dementia. We also found that chronic treatment with agmatine may improve amygdala-dependent emotional and spatial learning and memorial performance, and endothelial function, and may regulate eNOS and BDNF protein expression in aged rats.Conclusion: Results of the current study point out that chronic agmatine treatment may prevent endothelial dysfunction associated with vascular dementia through eNOS and BDNF expression in aged rats.
机译：目的：已经认识到生物衰老会引起记忆障碍和血管性痴呆的发展。根据我们之前的工作，已证明胍丁胺具有有益作用，并且可能对包括学习和记忆在内的认知功能具有治疗潜力。本研究的目的是探讨胍丁胺对大鼠生物衰老引起的血管内皮功能障碍和相关痴呆的可能作用。方法：我们使用了三个不同的年龄组（4月龄，18月龄和24岁） -月龄;对照组和胍丁胺治疗的大鼠中，每组n n ＝ 12。对照动物接受生理盐水8周。将硫酸胍丁胺（40？mg / kg，每天两次）口服给予胍丁胺组，持续8周。本文中，我们研究了胍丁胺对胸主动脉收缩压，一氧化氮介导的内皮依赖性和非依赖性血管舒张反应，认知能力（被动回避测试; PAT和莫里斯水迷宫测试;认知能力的影响）的影响。结果：我们发现老年大鼠认知能力下降，内皮功能障碍并降低eNOS和BDNF的表达。所有这些变化可能是由衰老引起的血管性痴呆引起的。我们还发现，胍丁胺的长期治疗可以改善杏仁核依赖性的情绪和空间学习和记忆能力以及内皮功能，并可能调节老年大鼠的eNOS和BDNF蛋白表达。结论：本研究的结果指出，慢性胍丁胺治疗可能通过衰老大鼠中的eNOS和BDNF表达来预防与血管性痴呆相关的内皮功能障碍。

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