Berberine extends healthspan and delays neurodegenerative diseases in Caenorhabditis elegans through ROS-dependent PMK-1/SKN-1 activation.

Yi Xiao, Li Zhang, Hanlin Zhou, Yingwen Cui, Keer Chen, Han Zhang, Qinyi Wu, Fang Liu

Institute of life sciences, Zunyi Medical University, Zunyi Guizhou 563000, China; College of Basic Medicine, Zunyi Medical University, Zunyi Guizhou563000, China. Electronic address: [email protected] of life sciences, Zunyi Medical University, Zunyi Guizhou 563000, China; College of Basic Medicine, Zunyi Medical University, Zunyi Guizhou563000, China. Electronic address: [email protected]. · pubmed

Paper

Abstract

Oxidative stress, or the chronic generation of reactive oxygen species (ROS), is thought to contribute to the progression of aging and aging related diseases. However, low degree of ROS generation has repeatedly been shown to be associated with beneficial outcomes via activation of protective signaling pathways. Berberine, a natural alkaloid isolated from Rhizomacoptidis, has a long history of medicinal use in both Ayurvedic and traditional Chinese medicine, which possesses anti-cancer, anti-inflammatory and anti-neurodegenerative properties. In this study, we utilize Caenorhabditis elegans to examine the mechanisms by which berberine influences healthspan and neurodegenerative diseases. We find that 10 μM berberine significantly extends healthy lifespan in wild type C. elegans. We further show that berberine generates ROS, which is followed by activation of PMK-1/SKN-1 to extend healthspan. Intriguingly, berberine also delays neurodegenerative diseases such as Alzheimer's and polyglutamine diseases in a PMK-1/SKN-1dependent manner. Our work suggests that berberine may be a viable candidate for the prevention and treatment of aging and aging related diseases.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the effects of berberine on healthspan and neurodegenerative diseases in C. elegans, focusing on mechanisms that may influence aging processes. It explores the activation of protective signaling pathways in response to ROS, which is relevant to understanding the biological mechanisms of aging. However, while the findings are solid and contribute to the understanding of potential interventions in aging, the study is limited in scope as it relies on a model organism and does not directly translate to human applications. Thus, it represents a solid research contribution but with limited immediate impact on the field of longevity research.

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