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Calycosin promotes lifespan in Caenorhabditis elegans through insulin signaling pathway via daf-16, age-1 and daf-2.
J Biosci Bioeng. 2017 Jul; 124(1):1-7.JB

Abstract

The naturally occurring calycosin is a known antioxidant that prevents redox imbalance in organisms. However, calycosin's effect on lifespan and its physiological molecular mechanisms are not yet well understood. In this study, we demonstrated that calycosin could prolong the lifespan of Caenorhabditis elegans, and that such extension was associated with its antioxidant capability as well as its ability to enhance stress resistance and reduce ROS (reactive oxygen species) accumulation. To explore mechanisms of this longevity effect, we assessed the impact of calycosin on lifespans of insulin-signaling impaired worms: daf-2, age-1, and daf-16 mutants. We found that calycosin did not alter the lifespan of all three mutants, thereby suggesting that calycosin requires insulin signaling to promote lifespan extension. On the other hand, we observed that calycosin could enhance the nuclear translocation of the core transcription factor DAF-16/FoXO instead of the conserved stress-responsive transcription factor SKN-1/Nrf-2. This observation is consistent with the understanding that the nuclear localized DAF-16 up-regulates its downstream targets sod-3, ctl-1, and hsp-16.2. Lastly, it is also noteworthy that the longevity effect of calycosin is likely not associated with the calorie restriction mechanism. Collectively, our results strongly suggest that calycosin could function as an antioxidant to extend the lifespan of C. elegans by enhancing nucleus translocation of DAF-16 through the insulin-signaling pathway.

Authors+Show Affiliations

Tianjin Key Laboratory for Modern Drug Delivery & High-Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, 92 Wei Jin Road, Tianjin 300072, PR China.Tianjin Key Laboratory for Modern Drug Delivery & High-Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, 92 Wei Jin Road, Tianjin 300072, PR China.Tianjin Key Laboratory for Modern Drug Delivery & High-Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, 92 Wei Jin Road, Tianjin 300072, PR China.Tianjin Key Laboratory for Modern Drug Delivery & High-Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, 92 Wei Jin Road, Tianjin 300072, PR China.Tianjin Key Laboratory for Modern Drug Delivery & High-Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, 92 Wei Jin Road, Tianjin 300072, PR China.Tianjin Key Laboratory for Modern Drug Delivery & High-Efficiency, School of Pharmaceutical Science and Technology, Tianjin University, 92 Wei Jin Road, Tianjin 300072, PR China. Electronic address: lijunzhou@tju.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28434978

Citation

Lu, Lulu, et al. "Calycosin Promotes Lifespan in Caenorhabditis Elegans Through Insulin Signaling Pathway Via Daf-16, Age-1 and Daf-2." Journal of Bioscience and Bioengineering, vol. 124, no. 1, 2017, pp. 1-7.
Lu L, Zhao X, Zhang J, et al. Calycosin promotes lifespan in Caenorhabditis elegans through insulin signaling pathway via daf-16, age-1 and daf-2. J Biosci Bioeng. 2017;124(1):1-7.
Lu, L., Zhao, X., Zhang, J., Li, M., Qi, Y., & Zhou, L. (2017). Calycosin promotes lifespan in Caenorhabditis elegans through insulin signaling pathway via daf-16, age-1 and daf-2. Journal of Bioscience and Bioengineering, 124(1), 1-7. https://doi.org/10.1016/j.jbiosc.2017.02.021
Lu L, et al. Calycosin Promotes Lifespan in Caenorhabditis Elegans Through Insulin Signaling Pathway Via Daf-16, Age-1 and Daf-2. J Biosci Bioeng. 2017;124(1):1-7. PubMed PMID: 28434978.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calycosin promotes lifespan in Caenorhabditis elegans through insulin signaling pathway via daf-16, age-1 and daf-2. AU - Lu,Lulu, AU - Zhao,Xuan, AU - Zhang,Jianyong, AU - Li,Miao, AU - Qi,Yonghao, AU - Zhou,Lijun, Y1 - 2017/04/20/ PY - 2016/11/01/received PY - 2017/02/21/accepted PY - 2017/4/25/pubmed PY - 2018/1/5/medline PY - 2017/4/25/entrez KW - Caenorhabditis elegans KW - Calycosin KW - DAF-16 KW - Insulin-signaling pathway KW - Lifespan KW - Reactive oxygen species SP - 1 EP - 7 JF - Journal of bioscience and bioengineering JO - J. Biosci. Bioeng. VL - 124 IS - 1 N2 - The naturally occurring calycosin is a known antioxidant that prevents redox imbalance in organisms. However, calycosin's effect on lifespan and its physiological molecular mechanisms are not yet well understood. In this study, we demonstrated that calycosin could prolong the lifespan of Caenorhabditis elegans, and that such extension was associated with its antioxidant capability as well as its ability to enhance stress resistance and reduce ROS (reactive oxygen species) accumulation. To explore mechanisms of this longevity effect, we assessed the impact of calycosin on lifespans of insulin-signaling impaired worms: daf-2, age-1, and daf-16 mutants. We found that calycosin did not alter the lifespan of all three mutants, thereby suggesting that calycosin requires insulin signaling to promote lifespan extension. On the other hand, we observed that calycosin could enhance the nuclear translocation of the core transcription factor DAF-16/FoXO instead of the conserved stress-responsive transcription factor SKN-1/Nrf-2. This observation is consistent with the understanding that the nuclear localized DAF-16 up-regulates its downstream targets sod-3, ctl-1, and hsp-16.2. Lastly, it is also noteworthy that the longevity effect of calycosin is likely not associated with the calorie restriction mechanism. Collectively, our results strongly suggest that calycosin could function as an antioxidant to extend the lifespan of C. elegans by enhancing nucleus translocation of DAF-16 through the insulin-signaling pathway. SN - 1347-4421 UR - https://www.unboundmedicine.com/medline/citation/28434978/Calycosin_promotes_lifespan_in_Caenorhabditis_elegans_through_insulin_signaling_pathway_via_daf_16_age_1_and_daf_2_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1389-1723(16)30470-4 DB - PRIME DP - Unbound Medicine ER -