Abstract

The increased prevalence of cognitive impairment, specifically among the aging population, has attracted attention in recent years. Trans-cinnamaldehyde (TCA), which is isolated from cinnamon, has recently drawn attention because of its potent anti-inflammatory and antioxidant properties. This study aimed to investigate the effects of TCA on learning and memory using a mouse model of cognitive impairment induced by a combination of D-galactose (D-gal) and aluminum chloride (AlCl₃). TCA (10 and 30 mg/kg/day) was administered orally for 30 days after the induction of cognitive impairment. The Morris water maze (MWM) task was performed to directly evaluate the neuroprotective effects of TCA on memory and spatial learning abilities. We found that TCA treatment attenuated cognitive impairment and reduced brain damage in the D‑gal- and AlCl₃-treated mice. To further investigate the mechanisms involved in the effects of TCA, we analyzed the nuclear factor erythroid 2-related factor (Nrf2) and related signaling pathways. We found that TCA upregulated AMP-activated protein kinase (AMPK), Nrf2, heme oxygenase 1 (HO-1) and NAD(P)H dehydrogenase [quinone] 1 (NQO-1); this suggests that TCA may attenuate cognitive dysfunction by reducing oxidative stress. We concluded that TCA reduced D-gal and AlCl₃-induced cognitive dysfunction through activation of the AMPK-mediated Nrf2/HO-1 signaling pathway in the brain. These results suggest that TCA may be a candidate for treating age-associated cognitive impairment.

中文翻译：

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反式肉桂醛对D-半乳糖和氯化铝诱导的小鼠认知功能障碍的保护作用

摘要

近年来，尤其是在老龄人口中，认知障碍的患病率上升已引起关注。从肉桂中分离出来的反式肉桂醛（TCA）最近因其有效的抗炎和抗氧化特性而受到关注。这项研究旨在使用D-半乳糖（D-gal）和氯化铝（AlCl ₃）。诱发认知障碍后，连续30天口服TCA（10和30 mg / kg /天）。进行了莫里斯水迷宫（MWM）任务，以直接评估TCA对记忆和空间学习能力的神经保护作用。我们发现，TCA治疗可减轻D‑gal-和AlCl ₃中的认知障碍并减少脑损伤治疗的小鼠。为了进一步研究参与TCA效应的机制，我们分析了核因子红系2相关因子（Nrf2）和相关的信号通路。我们发现，TCA上调了AMP激活的蛋白激酶（AMPK），Nrf2，血红素加氧酶1（HO-1）和NAD（P）H脱氢酶[醌] 1（NQO-1）。这表明TCA可以通过降低氧化应激来减轻认知功能障碍。我们得出的结论是，TCA通过激活脑中AMPK介导的Nrf2 / HO-1信号通路减少了D-gal和AlCl ₃诱导的认知功能障碍。这些结果表明，TCA可能是治疗与年龄相关的认知障碍的候选人。