This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: The authors confirm that all data underlying the findings are fully available without restriction. Received: JAccepted: OctoPublished: December 18, 2014Ĭopyright: © 2014 He et al. Kim, Stanford University Medical Center, United States of America (2014) Enhanced Longevity by Ibuprofen, Conserved in Multiple Species, Occurs in Yeast through Inhibition of Tryptophan Import. These results point to fundamental cell cycle signatures linked with longevity, implicate aromatic amino acid import in aging and identify a largely safe drug that extends lifespan across different kingdoms of life.Ĭitation: He C, Tsuchiyama SK, Nguyen QT, Plyusnina EN, Terrill SR, Sahibzada S, et al. Similar changes in cell cycle progression were evident in a large dataset of replicatively long-lived yeast deletion strains. Concomitant with lifespan extension, ibuprofen moderately reduced cell size at birth, leading to a delay in the G1 phase of the cell cycle. Loss of Tat2p increased replicative lifespan (RLS), but ibuprofen did not increase RLS when Tat2p was stabilized or in an already long-lived strain background impaired for aromatic amino acid uptake. Studies in yeast indicate that ibuprofen destabilizes the Tat2p permease and inhibits tryptophan uptake. Here we show that ibuprofen increased the lifespan of Saccharomyces cerevisiae, Caenorhabditis elegans and Drosophila melanogaster, indicative of conserved eukaryotic longevity effects.
However, a general pro-longevity role for ibuprofen and its mechanistic basis remains unclear. The common non-steroidal anti-inflammatory drug ibuprofen has been associated with a reduced risk of some age-related pathologies.