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      Bark Extract of the Amazonian Tree Endopleura uchi (Humiriaceae) Extends Lifespan and Enhances Stress Resistance in Caenorhabditis elegans

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          Abstract

          Endopleura uchi (Huber) Cuatrec (Humiriaceae), known as uxi or uxi-amarelo in Brazil, is an endemic tree of the Amazon forest. In traditional medicine, its stem bark is used to treat a variety of health disorders, including cancer, diabetes, arthritis, uterine inflammation, and gynecological infections. According to HPLC analysis, the main constituent of the bark extract is the polyphenol bergenin. In the current study, we demonstrate by in vitro and in vivo experiments the antioxidant potential of a water extract from the stem bark of E. uchi. When tested in the model organism Caenorhabditis elegans, the extract enhanced stress resistance via the DAF-16/FOXO pathway. Additionally, the extract promoted an increase in the lifespan of the worms independent from caloric restriction. It also attenuated the age-related muscle function decline and formation of polyQ40 plaques, as a model for Huntington’s disease. Thus, these data support anti-aging and anti-oxidant properties of E. uchi, which has not yet been described. More studies are needed to assess the real benefits of E. uchi bark for human health and its toxicological profile.

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          Most cited references37

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          Oxidative Stress, Mitochondrial Dysfunction, and Aging

          Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.
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            Polyphenols: antioxidants and beyond

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              Uncoupling lifespan and healthspan in Caenorhabditis elegans longevity mutants.

              Aging research has been very successful at identifying signaling pathways and evolutionarily conserved genes that extend lifespan with the assumption that an increase in lifespan will also increase healthspan. However, it is largely unknown whether we are extending the healthy time of life or simply prolonging a period of frailty with increased incidence of age-associated diseases. Here we use Caenorhabditis elegans, one of the premiere systems for lifespan studies, to determine whether lifespan and healthspan are intrinsically correlated. We conducted multiple cellular and organismal assays on wild type as well as four long-lived mutants (insulin/insulin-like growth factor-1, dietary restriction, protein translation, mitochondrial signaling) in a longitudinal manner to determine the health of the animals as they age. We find that some long-lived mutants performed better than wild type when measured chronologically (number of days). However, all long-lived mutants increased the proportion of time spent in a frail state. Together, these data suggest that lifespan can no longer be the sole parameter of interest and reveal the importance of evaluating multiple healthspan parameters for future studies on antiaging interventions.
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                Author and article information

                Contributors
                Role: Academic Editor
                Role: Academic Editor
                Journal
                Molecules
                Molecules
                molecules
                Molecules
                MDPI
                1420-3049
                06 March 2019
                March 2019
                : 24
                : 5
                : 915
                Affiliations
                [1 ]Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, INF 364, D-69120 Heidelberg, Germany; hspeixoto1@ 123456gmail.com (H.P.); marianaroxocorreia@ 123456gmail.com (M.R.); markus.braun@ 123456gmx.ch (M.B.); wxjsz@ 123456hotmail.com (X.W.)
                [2 ]Faculty of Pharmaceutical Science, Federal University of Amazonas (UFAM), 6200 General Rodrigo, Manaus 69077-000, Brazil; eslima75@ 123456gmail.com (E.S.); karlaacussena@ 123456gmail.com (K.V.)
                Author notes
                [* ]Correspondence: wink@ 123456uni-heidelberg.de ; Tel.: +49-62-2154-4880
                Author information
                https://orcid.org/0000-0001-5538-0141
                https://orcid.org/0000-0001-6063-8303
                https://orcid.org/0000-0002-7875-4510
                Article
                molecules-24-00915
                10.3390/molecules24050915
                6429406
                30845642
                7cbe793e-a503-4a98-a133-99cb3b32b0bb
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 06 February 2019
                : 01 March 2019
                Categories
                Article

                caenorhabditis elegans,antioxidants,bergenin,stress resistance,lifespan,huntington,uxi,endopleura uchi

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