Epigallocatechin-3-gallate promotes healthy lifespan through mitohormesis during early-to-mid adulthood in Caenorhabditis elegans
| Autor: | Jianan Huang, Yi-Jun Chen, Jie-Wen Tong, Yushun Gong, Li-Gui Xiong, Zhonghua Liu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
AMPK Aging media_common.quotation_subject Clinical Biochemistry Dietary supplement Longevity Early-to-mid adulthood Biochemistry complex mixtures Catechin 03 medical and health sciences Mitohormesis Animals heterocyclic compounds Caenorhabditis elegans lcsh:QH301-705.5 media_common chemistry.chemical_classification Reactive oxygen species lcsh:R5-920 Organelle Biogenesis biology Epigallocatechin-3-gallate Tea Organic Chemistry food and beverages biology.organism_classification Cell biology Mitochondria 030104 developmental biology Mitochondrial biogenesis chemistry lcsh:Biology (General) Younger adults C. elegans Healthy lifespan sense organs lcsh:Medicine (General) Reactive Oxygen Species Function (biology) Research Paper |
| Zdroj: | Redox Biology Redox Biology, Vol 14, Iss, Pp 305-315 (2018) |
| ISSN: | 2213-2317 |
| Popis: | The green tea polyphenol epigallocatechin-3-gallate (EGCG) is widely consumed as a dietary supplement. Its potential properties include slowing aging and extending lifespan, although how exactly this is achieved remains unclear. Here, we report that EGCG promoted healthy lifespan in Caenorhabditis elegans when administered throughout or only at early-to-mid adulthood. Specifically, EGCG extended lifespan in an inverted U-shaped dose-response manner. The life-extending mechanism was stimulated by EGCG-induced production of reactive oxygen species (ROS). Additionally, EGCG triggered mitochondrial biogenesis to restore mitochondrial function. The EGCG-induced increase in lifespan depends on known energy sensors such as AMPK/AAK-2, as well as SIRT1/SIR-2.1 and FOXO/DAF-16. Interestingly, aging decreased the response to EGCG and progressively neutralized its beneficial effects on longevity. Collectively, our findings link EGCG to the process of mitohormesis and suggest an inducible, AMPK/SIRT1/FOXO-dependent redox signaling module that could be invoked in different contexts to extend healthy lifespan. Its effectiveness is higher in younger adults and declines with age. Graphical abstract fx1 Highlights • EGCG promoted healthy lifespan at early-to-mid adulthood. • The life-extending mechanism of EGCG involved the process of mitohormesis. • EGCG triggered mitochondrial biogenesis to restore mitochondrial function. • Promotion of longevity due to EGCG occur dependent on AAK-2/SIR-2.1/DAF-16. • Aging progressively blunted the EGCG beneficial effects to longevity. |
| Databáze: | OpenAIRE |
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