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      Honey and its nutritional and anti-inflammatory value

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          Abstract

          Inflammation is the main key role in developing chronic diseases including cancer, cardiovascular diseases, diabetes, arthritis, and neurodegenerative diseases which possess a huge challenge for treatment. With massively compelling evidence of the role played by nutritional modulation in preventing inflammation-related diseases, there is a growing interest into the search for natural functional foods with therapeutic and preventive actions. Honey, a nutritional healthy product, is produced mainly by two types of bees: honeybee and stingless bee. Since both types of honey possess distinctive phenolic and flavonoid compounds, there is recently an intensive interest in their biological and clinical actions against inflammation-mediated chronic diseases. This review shed the light specifically on the bioavailability and bioaccessibility of honey polyphenols and highlight their roles in targeting inflammatory pathways in gastrointestinal tract disorders, edema, cancer, metabolic and cardiovascular diseases and gut microbiota.

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          Most cited references137

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          ROS function in redox signaling and oxidative stress.

          Oxidative stress refers to elevated intracellular levels of reactive oxygen species (ROS) that cause damage to lipids, proteins and DNA. Oxidative stress has been linked to a myriad of pathologies. However, elevated ROS also act as signaling molecules in the maintenance of physiological functions--a process termed redox biology. In this review we discuss the two faces of ROS--redox biology and oxidative stress--and their contribution to both physiological and pathological conditions. Redox biology involves a small increase in ROS levels that activates signaling pathways to initiate biological processes, while oxidative stress denotes high levels of ROS that result in damage to DNA, protein or lipids. Thus, the response to ROS displays hormesis, given that the opposite effect is observed at low levels compared with that seen at high levels. Here, we argue that redox biology, rather than oxidative stress, underlies physiological and pathological conditions. Copyright © 2014 Elsevier Ltd. All rights reserved.
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            ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis.

            Reactive oxygen species (ROS) have been shown to be toxic but also function as signalling molecules. This biological paradox underlies mechanisms that are important for the integrity and fitness of living organisms and their ageing. The pathways that regulate ROS homeostasis are crucial for mitigating the toxicity of ROS and provide strong evidence about specificity in ROS signalling. By taking advantage of the chemistry of ROS, highly specific mechanisms have evolved that form the basis of oxidant scavenging and ROS signalling systems.
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              Oxidative stress, inflammation, and cancer: how are they linked?

              Extensive research during the past 2 decades has revealed the mechanism by which continued oxidative stress can lead to chronic inflammation, which in turn could mediate most chronic diseases including cancer, diabetes, and cardiovascular, neurological, and pulmonary diseases. Oxidative stress can activate a variety of transcription factors including NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2. Activation of these transcription factors can lead to the expression of over 500 different genes, including those for growth factors, inflammatory cytokines, chemokines, cell cycle regulatory molecules, and anti-inflammatory molecules. How oxidative stress activates inflammatory pathways leading to transformation of a normal cell to tumor cell, tumor cell survival, proliferation, chemoresistance, radioresistance, invasion, angiogenesis, and stem cell survival is the focus of this review. Overall, observations to date suggest that oxidative stress, chronic inflammation, and cancer are closely linked. Copyright © 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                abdah@upm.edu.my
                Journal
                BMC Complement Med Ther
                BMC Complement Med Ther
                BMC Complementary Medicine and Therapies
                BioMed Central (London )
                2662-7671
                14 January 2021
                14 January 2021
                2021
                : 21
                : 30
                Affiliations
                [1 ]GRID grid.444483.b, ISNI 0000 0001 0694 3091, Department of Technology and Natural Resources, Faculty of Applied Sciences and Technology, , Universiti Tun Hussein Onn Malaysia, ; 86400 Pagoh, Johor Malaysia
                [2 ]GRID grid.11142.37, ISNI 0000 0001 2231 800X, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, , Universiti Putra Malaysia, ; 43400 UPM Serdang, Selangor Malaysia
                [3 ]GRID grid.4425.7, ISNI 0000 0004 0368 0654, Sport and Exercises Sciences School, Faculty of Science, , Liverpool John Moores University, ; Liverpool, UK
                [4 ]GRID grid.472319.a, ISNI 0000 0001 0708 9739, Department of Forensic Biology, Faculty of Forensic Sciences, , Naif Arab University of Security Sciences, ; Riyadh, 14812 Saudi Arabia
                Author information
                http://orcid.org/0000-0001-5989-5804
                Article
                3170
                10.1186/s12906-020-03170-5
                7807510
                33441127
                ae7215a9-f744-4b16-92bc-40b0bc1b9bd8
                © The Author(s) 2021

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 8 July 2020
                : 29 November 2020
                Funding
                Funded by: Universiti Putra Malaysia (MY)
                Award ID: Research Grant Number: 05-01-11-1218RU
                Categories
                Review
                Custom metadata
                © The Author(s) 2021

                honey,chronic inflammation,bioavailability,bioaccessibility,bioactive compounds

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