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膳食肉桂通过mTORC1和自噬信号通路促进长寿并延长健康寿命。

Dietary cinnamon promotes longevity and extends healthspan via mTORC1 and autophagy signaling.

作者信息

Guo Yuling, Zhang Qing, Zhang Bi, Pan Tong, Ronan Elizabeth A, Huffman Anthony, He Yongqun, Inoki Ken, Liu Jianfeng, Xu X Z Shawn

机构信息

College of Life Science and Technology, Key Laboratory of Molecular Biophysics of MOE, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA.

出版信息

Aging Cell. 2025 Apr;24(4):e14448. doi: 10.1111/acel.14448. Epub 2025 Jan 6.

DOI:10.1111/acel.14448
PMID:39760475
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11984692/
Abstract

Cinnamon, renowned for its aromatic flavor, represents one of the most widely used spices worldwide. Cinnamon is also considered beneficial to human health with therapeutic potential for treating various diseases, ranging from diabetes and cancer to neurodegenerative diseases. However, the mechanisms underlying cinnamon's health benefits remain elusive. It is also unclear whether cinnamon has any role in aging. Using C. elegans as a model, here we show that feeding worms cinnamaldehyde (CA), the active ingredient in cinnamon oil, prolongs longevity. CA also promotes stress resistance and reduces β-Amyloid toxicity in a C. elegans model of Alzheimer's disease. Mechanistically, CA exerts its beneficial effects through mTORC1 and autophagy signaling. Interestingly, CA promotes longevity by inducing a dietary restriction-like state without affecting food intake, suggesting CA as a dietary restriction mimetic. In human cells, CA exerts a similar effect on mTORC1 and autophagy signaling, suggesting a conserved mechanism. Our results demonstrate that dietary cinnamon promotes both lifespan and healthspan and does so by regulating mTORC1 and autophagy signaling.

摘要

肉桂以其芳香的味道而闻名,是世界上使用最广泛的香料之一。肉桂也被认为对人体健康有益,具有治疗多种疾病的潜力,从糖尿病、癌症到神经退行性疾病。然而,肉桂对健康有益的潜在机制仍然难以捉摸。肉桂是否在衰老过程中发挥作用也不清楚。以秀丽隐杆线虫为模型,我们在此表明,给线虫喂食肉桂油中的活性成分肉桂醛(CA)可延长寿命。在阿尔茨海默病的秀丽隐杆线虫模型中,CA还能增强抗逆性并降低β-淀粉样蛋白毒性。从机制上讲,CA通过mTORC1和自噬信号发挥其有益作用。有趣的是,CA通过诱导类似饮食限制的状态来延长寿命,而不影响食物摄入量,这表明CA可模拟饮食限制。在人类细胞中,CA对mTORC1和自噬信号也有类似作用,表明存在保守机制。我们的结果表明,食用肉桂可延长寿命并促进健康,其作用机制是通过调节mTORC1和自噬信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/20a820f06677/ACEL-24-e14448-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/1af7e4c4a333/ACEL-24-e14448-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/afd516f17dd1/ACEL-24-e14448-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/c4b60eb6a5d5/ACEL-24-e14448-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/a6ca443752e6/ACEL-24-e14448-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/28629f31f6ff/ACEL-24-e14448-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/20a820f06677/ACEL-24-e14448-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/1af7e4c4a333/ACEL-24-e14448-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/afd516f17dd1/ACEL-24-e14448-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/c4b60eb6a5d5/ACEL-24-e14448-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/a6ca443752e6/ACEL-24-e14448-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/28629f31f6ff/ACEL-24-e14448-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0327/11984692/20a820f06677/ACEL-24-e14448-g006.jpg

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本文引用的文献

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