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      New highlights on the health-improving effects of sulforaphane

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          Abstract

          In this paper, we review recent evidence about the beneficial effects of sulforaphane (SFN), which is the most studied member of isothiocyanates, on both in vivo and in vitro models of different diseases, mainly diabetes and cancer.

          Abstract

          In this paper, we review recent evidence about the beneficial effects of sulforaphane (SFN), which is the most studied member of isothiocyanates, on both in vivo and in vitro models of different diseases, mainly diabetes and cancer. The role of SFN on oxidative stress, inflammation, and metabolism is discussed, with emphasis on those nuclear factor E2-related factor 2 (Nrf2) pathway-mediated mechanisms. In the case of the anti-inflammatory effects of SFN, the point of convergence seems to be the downregulation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), with the consequent amelioration of other pathogenic processes such as hypertrophy and fibrosis. We emphasized that SFN shows opposite effects in normal and cancer cells at many levels; for instance, while in normal cells it has protective actions, in cancer cells it blocks the induction of factors related to the malignity of tumors, diminishes their development, and induces cell death. SFN is able to promote apoptosis in cancer cells by many mechanisms, the production of reactive oxygen species being one of the most relevant ones. Given its properties, SFN could be considered as a phytochemical at the forefront of natural medicine.

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          Most cited references 146

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          NF-kappaB: linking inflammation and immunity to cancer development and progression.

          There has been much effort recently to probe the long-recognized relationship between the pathological processes of infection, inflammation and cancer. For example, epidemiological studies have shown that approximately 15% of human deaths from cancer are associated with chronic viral or bacterial infections. This Review focuses on the molecular mechanisms that connect infection, inflammation and cancer, and it puts forward the hypothesis that activation of nuclear factor-kappaB (NF-kappaB) by the classical, IKK-beta (inhibitor-of-NF-kappaB kinase-beta)-dependent pathway is a crucial mediator of inflammation-induced tumour growth and progression, as well as an important modulator of tumour surveillance and rejection.
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            Endoplasmic reticulum stress: cell life and death decisions.

            Disturbances in the normal functions of the ER lead to an evolutionarily conserved cell stress response, the unfolded protein response, which is aimed initially at compensating for damage but can eventually trigger cell death if ER dysfunction is severe or prolonged. The mechanisms by which ER stress leads to cell death remain enigmatic, with multiple potential participants described but little clarity about which specific death effectors dominate in particular cellular contexts. Important roles for ER-initiated cell death pathways have been recognized for several diseases, including hypoxia, ischemia/reperfusion injury, neurodegeneration, heart disease, and diabetes.
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              Introduction to NF-kappaB: players, pathways, perspectives.

               Ian Gilmore (2006)
              This article serves as an introduction to the collection of reviews on nuclear factor-kappaB (NF-kappaB). It provides an overview of the discovery and current status of NF-kappaB as a research topic. Described are the structures, activities and regulation of the proteins in the NF-kappaB family of transcription factors. NF-kappaB signaling is primarily regulated by inhibitor kappaB (IkappaB) proteins and the IkappaB kinase complex through two major pathways: the canonical and non-canonical NF-kappaB pathways. The organization and focus of articles included in the following reviews are described, as well as likely future areas of research interest on NF-kappaB.
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                Author and article information

                Journal
                FFOUAI
                Food & Function
                Food Funct.
                Royal Society of Chemistry (RSC)
                2042-6496
                2042-650X
                2018
                2018
                : 9
                : 5
                : 2589-2606
                Affiliations
                [1 ]Departamento de Biología
                [2 ]Facultad de Química
                [3 ]Universidad Nacional Autónoma de México
                [4 ]Mexico City 04510
                [5 ]Mexico
                [6 ]National Council of Science and Technology – National Institute of Cardiology Ignacio Chávez
                [7 ]Mexico City 14080
                Article
                10.1039/C8FO00018B
                © 2018

                http://rsc.li/journals-terms-of-use

                Product
                Self URI (article page): http://xlink.rsc.org/?DOI=C8FO00018B

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