Journal of Chinese Pharmaceutical Sciences ›› 2016, Vol. 25 ›› Issue (8): 605-613.DOI: 10.5246/jcps.2016.08.068

• Original articles • Previous Articles     Next Articles

Cinnamaldehyde promotes mitochondrial function and reduces Aβ toxicity in neural cells

Lidan Bai1, Xue Li1, Qing Chang2, Rui Wu2, Jing Zhang2*, Xiaoda Yang1,3*   

  1. 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:,
  • Supported by:
    National Natural Science Foundation of China (Grant No. 21571006 and 21271012) and Beijing Natural Science Foundation (Grant No. 7164308).


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 (ΔΨm), 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

CLC Number: