中文摘要：

一些研究表明肉桂及其主要活性成分肉桂醛具有抗阿尔兹海默症（AD）活性。为了阐明肉桂醛的作用机制、促进抗AD药物开发,本文研究了肉桂醛对SH-SY5Y神经细胞特别是线粒体的作用。实验结果表明,肉桂醛能够促进神经细胞在有和无β-淀粉状蛋白（Aβ）负载下的细胞活力,其作用机制包括：保护和恢复Aβ损伤的正常线粒体形态、维持线粒体膜电位和降低ROS的产生。肉桂醛导致Drp1蛋白表达可能与其阻止Aβ诱导线粒体裂解有关。此外,肉桂醛也能抑制Aβ的寡聚化,降低其细胞毒性。但肉桂醛对SH-SY5Y神经细胞Tau蛋白的磷酸化却没有明显作用。总之,肉桂醛可促进神经细胞线粒体功能并抑制Aβ毒性,这两个机制在神经保护方面互相关联。本文结果提示肉桂醛可以作为保健药物用于AD和其他衰老性代谢疾病的防治。

英文摘要：

Cinnamon and its major active component, cinnamaldehyde, have been shown to be neuroprotective in models of Alzheimer＇s disease （AD）. To further investigate the mechanism of cinnamaldehyde, we investigated the effects of cinnamaldehyde focusing on mitochondrial function in SH-SYSY neural cells. The results demonstrated that cinnamaldehyde could enhance neural cell viability with or without increased Aβ levels. Cinnamaldehyde facilitated the maintenance of normal mitochondrial morphology, preserved the mitochondrial membrane potential （ATm）, and reduced production of reactive oxygen species （ROS）. Cinnamaldehyde also decreased the expression of dynamin-related protein 1 （Drpl）, a protein critically involved in mitochondrial dynamics. In addition, cinnamaldehyde inhibited Aβ oligomerization, but it had no effects on Tau phosphorylation. In overall, cinnamaldehyde promoted mitochondrial function and inhibited Aβ toxicity, and these two properties may both contribute to the neuroprotective effect. These results suggest that cinnamaldehyde could be a potential nutriceutical in the prevention and even therapeutic treatment of AD as well as other aging-related metabolic syndromes.