肉桂醛促进神经细胞线粒体功能并抑制Aβ毒性

doi:10.5246/jcps.2016.08.068

中国药学(英文版) ›› 2016, Vol. 25 ›› Issue (8): 605-613.DOI: 10.5246/jcps.2016.08.068

肉桂醛促进神经细胞线粒体功能并抑制Aβ毒性

白力丹¹, 李雪¹, 常青², 武睿², 章京^2*, 杨晓达^1,3*

1. 北京大学医学部药学院天然药物及仿生药物国家重点实验室; 化学生物学系, 北京 100191
2. 北京大学医学部基础医学院病理学系, 北京 100191
3. 国家中医药管理局中药复方解毒重点研究室, 北京 100191

收稿日期:2016-04-20 修回日期:2016-05-13 出版日期:2016-09-01 发布日期:2016-05-23
通讯作者: Tel.: +86-010-82805611, E-mail: xyang@bjmu.edu.cn, zhangjing6202@163.com
基金资助:
National Natural Science Foundation of China (Grant No. 21571006 and 21271012) and Beijing Natural Science Foundation (Grant No. 7164308).

Cinnamaldehyde promotes mitochondrial function and reduces Aβ toxicity in neural cells

Lidan Bai¹, Xue Li¹, Qing Chang², Rui Wu², Jing Zhang^2*, Xiaoda Yang^1,3*

1. State Key Laboratories of Natural and Biomimetic Drugs; Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100191, China
2. Department of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China
3. SATCM Key Laboratory of Compound Drug Detoxication at Peking University, Beijing 100191, China

Received:2016-04-20 Revised:2016-05-13 Online:2016-09-01 Published:2016-05-23
Contact: Tel.: +86-010-82805611, E-mail: xyang@bjmu.edu.cn, zhangjing6202@163.com
Supported by:
National Natural Science Foundation of China (Grant No. 21571006 and 21271012) and Beijing Natural Science Foundation (Grant No. 7164308).

摘要/Abstract

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。

关键词: 阿尔茨海默症, β样淀粉蛋白, 线粒体, 肉桂醛

Abstract:

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-SY5Y 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 (ΔΨ_m), and reduced production of reactive oxygen species (ROS). Cinnamaldehyde also decreased the expression of dynamin-related protein 1 (Drp1), 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.

Key words: Alzheimer’s disease, A&beta, oligomers, Mitochondria, Cinnamaldehyde

中图分类号:

R962

Supporting:

白力丹, 李雪, 常青, 武睿, 章京, 杨晓达. 肉桂醛促进神经细胞线粒体功能并抑制Aβ毒性[J]. 中国药学(英文版), 2016, 25(8): 605-613.

Lidan Bai, Xue Li, Qing Chang, Rui Wu, Jing Zhang, Xiaoda Yang. Cinnamaldehyde promotes mitochondrial function and reduces Aβ toxicity in neural cells[J]. Journal of Chinese Pharmaceutical Sciences, 2016, 25(8): 605-613.

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肉桂醛促进神经细胞线粒体功能并抑制Aβ毒性

Cinnamaldehyde promotes mitochondrial function and reduces Aβ toxicity in neural cells

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