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      Curcumin in Cell Death Processes: A Challenge for CAM of Age-Related Pathologies

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          Abstract

          Curcumin, the yellow pigment from the rhizoma of Curcuma longa, is a widely studied phytochemical which has a variety of biological activities: anti-inflammatory and anti-oxidative. In this review we discuss the biological mechanisms and possible clinical effects of curcumin treatment on cancer therapy, and neurodegenerative diseases such as Alzheimer's Disease, with particular attention to the cell death processes induced by curcumin. Since oxidative stress and inflammation are major determinants of the aging process, we also argue that curcumin can have a more general effect that slows down the rate of aging. Finally, the effects of curcumin can be described as xenohormetic, since it activates a sort of stress response in mammalian cells.

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          Inflamm-aging. An evolutionary perspective on immunosenescence.

          C Franceschi, M BonaFe, S Valensin … (2000)
          In this paper we extend the "network theory of aging," and we argue that a global reduction in the capacity to cope with a variety of stressors and a concomitant progressive increase in proinflammatory status are major characteristics of the aging process. This phenomenon, which we will refer to as "inflamm-aging," is provoked by a continuous antigenic load and stress. On the basis of evolutionary studies, we also argue that the immune and the stress responses are equivalent and that antigens are nothing other than particular types of stressors. We also propose to return macrophage to its rightful place as central actor not only in the inflammatory response and immunity, but also in the stress response. The rate of reaching the threshold of proinflammatory status over which diseases/disabilities ensue and the individual capacity to cope with and adapt to stressors are assumed to be complex traits with a genetic component. Finally, we argue that the persistence of inflammatory stimuli over time represents the biologic background (first hit) favoring the susceptibility to age-related diseases/disabilities. A second hit (absence of robust gene variants and/or presence of frail gene variants) is likely necessary to develop overt organ-specific age-related diseases having an inflammatory pathogenesis, such as atherosclerosis, Alzheimer's disease, osteoporosis, and diabetes. Following this perspective, several paradoxes of healthy centenarians (increase of plasma levels of inflammatory cytokines, acute phase proteins, and coagulation factors) are illustrated and explained. In conclusion, the beneficial effects of inflammation devoted to the neutralization of dangerous/harmful agents early in life and in adulthood become detrimental late in life in a period largely not foreseen by evolution, according to the antagonistic pleiotropy theory of aging.
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            Multiple biological activities of curcumin: a short review.

            Radha K Maheshwari, Anoop Singh, Jaya P Gaddipati … (2006)
            Turmeric (Curcuma longa rhizomes), commonly used as a spice is well documented for its medicinal properties in Indian and Chinese systems of medicine. It has been widely used for the treatment of several diseases. Epidemiological observations, though inconclusive, are suggestive that turmeric consumption may reduce the risk of some form of cancers and render other protective biological effects in humans. These biological effects of turmeric have been attributed to its constituent curcumin that has been widely studied for its anti-inflammatory, anti-angiogenic, anti-oxidant, wound healing and anti-cancer effects. As a result of extensive epidemiological, clinical, and animal studies several molecular mechanisms are emerging that elucidate multiple biological effects of curcumin. This review summarizes the most interesting in vitro and in vivo studies on the biological effects of curcumin.
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              Curcumin activates the haem oxygenase-1 gene via regulation of Nrf2 and the antioxidant-responsive element.

              Elisabeth Balogun, Martha Hoque, Pengfei Gong … (2003)
              The transcription factor Nrf2, which normally exists in an inactive state as a consequence of binding to a cytoskeleton-associated protein Keap1, can be activated by redox-dependent stimuli. Alteration of the Nrf2-Keap1 interaction enables Nrf2 to translocate to the nucleus, bind to the antioxidant-responsive element (ARE) and initiate the transcription of genes coding for detoxifying enzymes and cytoprotective proteins. This response is also triggered by a class of electrophilic compounds including polyphenols and plant-derived constituents. Recently, the natural antioxidants curcumin and caffeic acid phenethyl ester (CAPE) have been identified as potent inducers of haem oxygenase-1 (HO-1), a redox-sensitive inducible protein that provides protection against various forms of stress. Here, we show that in renal epithelial cells both curcumin and CAPE stimulate the expression of Nrf2 in a concentration- and time-dependent manner. This effect was associated with a significant increase in HO-1 protein expression and haem oxygenase activity. From several lines of investigation we also report that curcumin (and, by inference, CAPE) stimulates ho-1 gene activity by promoting inactivation of the Nrf2-Keap1 complex, leading to increased Nrf2 binding to the resident ho-1 AREs. Moreover, using antibodies and specific inhibitors of the mitogen-activated protein kinase (MAPK) pathways, we provide data implicating p38 MAPK in curcumin-mediated ho-1 induction. Taken together, these results demonstrate that induction of HO-1 by curcumin and CAPE requires the activation of the Nrf2/ARE pathway.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Evid Based Complement Alternat Med
                Journal ID (publisher-id): eCAM
                Journal ID (publisher-id): Evidence-based Complementary and Alternative Medicine
                Title: Evidence-based Complementary and Alternative Medicine
                Publisher: Oxford University Press
                ISSN (Print): 1741-427X
                ISSN (Electronic): 1741-4288
                Publication date (Print): June 2007
                Publication date (Electronic): 23 April 2007
                Volume: 4
                Issue: 2
                Pages: 181-190
                Affiliations
                1Department of Experimental Pathology and Centro Interdipartimentale “L. Galvani”, University of Bologna, via S. Giacomo 12, 40126 Bologna, Italy, 2ER-GenTech laboratory, via Saragat 1, 44100 Ferrara, Italy, 3Department of Cellular Biochemistry, Nencki Institute of Experimental Biology, 3 Pasteura St., 02-093 Warsaw, Poland, 4Laboratory of Comparative Neuroimmunology, Department of Neurobiology, David Geffen School of Medicine at UCLA, University of California at Los Angeles, Los Angeles California 90095-1763 and 5I.N.R.C.A., Department of Gerontological Sciences, via Birarelli 8, 60121 Ancona, Italy
                Author notes
                For reprints and all correspondence: Prof. Claudio Franceschi, Department of Experimental Pathology and Centro Interdipartimentale “L. Galvani”, University of Bologna, via S. Giacomo 12, 40126 Bologna, Italy. E-mail: claudio.franceschi@ 123456unibo.it
                Article
                DOI: 10.1093/ecam/nem043
                PMC ID: 1876609
                PubMed ID: 17549234
                SO-VID: 544f9f4e-04be-4fc9-a1df-7eff45be7bc6
                Copyright © © 2007 The Author(s)
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 11 October 2006
                Date accepted : 24 March 2007
                Categories
                Subject: Reviews

                ScienceOpen disciplines: Complementary & Alternative medicine
                Keywords: neurodegenerative diseases,cancer,curcumin,xenohormesis,aging,apoptosis
                Data availability:
                ScienceOpen disciplines: Complementary & Alternative medicine
                Keywords: neurodegenerative diseases, cancer, curcumin, xenohormesis, aging, apoptosis

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