NF-κB activation in response to toxical and therapeutical agents: role in inflammation and cancer treatment

Bours, Vincent; Bonizzi, Giuseppina; Bentires‐Alj, Mohamed; Bureau, Fabrice; Piette, Jacques; Lekeux, Pierre; Merville, Marie Paule

doi:10.1016/s0300-483x(00)00302-4

Cited by 89 publications

(65 citation statements)

References 69 publications

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“…Astaxanthin is, indeed, a very potent antioxidant and free-radical scavenger [30,82,85], and oxidative stress is known to be implicated in the activation of NF-B [83,86,87].…”

Section: Discussionmentioning

confidence: 99%

The inhibition of TNF-α-induced NF-κB activation by marine natural products

Folmer

Jaspars

Solano

et al. 2009

Biochemical Pharmacology

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, et al.. The inhibition of TNF-α induced NF-κB activation by marine natural products. Biochemical Pharmacology, Elsevier, 2009, 78 (6) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 AbstractThe deregulated activation of NF-B is associated with cancer development and inflammatory diseases. With the aim to find new NF-B inhibitors, we purified and characterized compounds from extracts of the Fijian sponge Rhabdastrella globostellata, the crinoid Comanthus parvicirrus, the soft corals Sarcophyton sp. nov. and Sinularia sp., and the gorgonian Subergorgia sp. after an initial screening of 266 extracts from different marine origins.Results obtained show that selected purified compounds had a cytotoxic effect on the human leukaemia cell line K562, inhibited both TNF--induced NF-B-DNA binding as well as TNF- induced IB degradation and nuclear translocation of p50/p65. Furthermore, we observed inhibition of NF-B activation induced by an overexpression of TNFR1, TRAF2, TRADD, or IKK Interestingly, natural products inhibited IKK kinase as well as the 26S proteasome proteolytic activity.

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“…Astaxanthin is, indeed, a very potent antioxidant and free-radical scavenger [30,82,85], and oxidative stress is known to be implicated in the activation of NF-B [83,86,87].…”

Section: Discussionmentioning

confidence: 99%

The inhibition of TNF-α-induced NF-κB activation by marine natural products

Folmer

Jaspars

Solano

et al. 2009

Biochemical Pharmacology

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“…Hyperglycemia also causes oxidative stress due to the increased mitochondrial production of superoxide, including the depletion of NADPH and consequent disturbance of glutathione and nitric oxide metabolism. These oxidative stresses are responsible for regulation of the transcriptional pathways of NF-kB, 35) which is a transcription factor thought to play an important role in the onset of inflammation. 36) The activation of NF-kB by oxidative stress is induced by a cascade of events leading to the activation of inhibitor kB (IkB) kinase, which phosphorylates IkB, leading to its degradation and the translocation of NF-kB to the nucleus.…”

Section: Discussionmentioning

confidence: 99%

The Beneficial Effects of Morroniside on the Inflammatory Response and Lipid Metabolism in the Liver of <i>db</i>/<i>db</i> Mice

Park

Yamabe

Noh

et al. 2009

Biological & Pharmaceutical Bulletin

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Diabetes mellitus is a major cause of mortality and morbidity worldwide, and its prevalence is increasing at an alarming rate. Hyperglycemia and dyslipidemia lead to complications associated with diabetes mellitus, and, also, the attenuation of oxidative stress and regulation of stress-sensitive signaling pathways have been considered as ways to alleviate diabetes. [1][2][3][4] Hyperglycemia causes oxidative stress by two mechanisms: first, by decreasing the regeneration of the important cellular antioxidant, reduced glutathione (GSH) from oxidized glutathione (GSSG), and second, by decreasing the availability of reduced nicotinamide adenine dinucleotide phosphate (NADPH). Furthermore, hyperglycemia-induced reactive oxygen species (ROS) stimulate the activation of protein kinase C (PKC), formation of advanced glycation endproducts (AGE), and sorbitol accumulation. Also, increased ROS lead to the activation of nuclear factor-kappa B (NF-kB), and activated NF-kB can enhance the expression of proinflammatory cytokines, chemokines, adhesion molecules, inflammatory receptors, and inflammatory enzymes such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). 5-7)Dyslipidemia is the abnormal state of elevated cholesterol, triglyceride, and low-density lipoprotein or decreased highdensity lipoprotein in the plasma level that contribute to the development of atherosclerosis. Dyslipidemia is a risk factor for coronary artery disease, a leading cause of mortality in patients with diabetes mellitus. [8][9][10] Triglyceride is involved in the ectopic accumulation of lipid stores in the liver and are associated with a number of diseases such as metabolic syndrome and type 2 diabetes. Critical players in potentiating the promoting effect of hyperinsulinemia on hepatic lipid accumulation are the anabolic transcription factor peroxisome proliferator activated receptor a (PPARa) and sterol regulatory element binding proteins (SREBPs), which upregulate genes such as those for fatty acid synthase and cholesterol levels. [11][12][13] Corni Fructus (Cornus officinalis SIEB. et ZUCC.) is a rich source of iridoid glycosides in traditional medicine.14) Iridoids are a group of natural products belonging to the terpenoids, which are ubiquitous in plants. However, only a limited number of taxa possess the enzymes that give rise to the cyclopentane ring that is characteristic of the carbocyclic iridoids.15) Morroniside is a carbocyclic iridoid glycoside which has been reported to exhibit marked antioxidant activity. 16) In our previous studies, we reported the beneficial effect of morroniside on streptozotocin-induced type 1 diabetic renal damage. The administration of morroniside could ameliorate hyperglycemia, renal oxidative stress, and inflammation in diabetic rats. 17) However, the effect of morroniside on the type 2 diabetic liver, especially in dyslipidemia, has not yet been determined. The liver is an important organ for maintaining glucose metabolism and lipid homeostasis, since it can store (via glycogen synthes...

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“…A large number of NFkB-dependent genes have antiapoptotic functions. These include TNF receptor-associated factor 1 (TRAF1), TRAF2, cellular inhibitors of apoptosis proteins (CIAPs), MnSOD, and A20 zinc finger protein (reviewed in Pahl, 1999;Bours et al, 2000). NFkB is also involved in regulating the expression of Bf1-1/A1 and Bcl-XL, two anti-apoptotic members of the Bcl2 family.…”

Section: Nuclear Factor Kb (Nf Kb) Signalingmentioning

confidence: 99%

Cellular response to oxidative stress: Signaling for suicide and survival*

Martindale

Holbrook

2002

Journal Cellular Physiology

2,095

1,596

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Reactive oxygen species (ROS), whether produced endogenously as a consequence of normal cell functions or derived from external sources, pose a constant threat to cells living in an aerobic environment as they can result in severe damage to DNA, protein, and lipids. The importance of oxidative damage to the pathogenesis of many diseases as well as to degenerative processes of aging has becoming increasingly apparent over the past few years. Cells contain a number of antioxidant defenses to minimize fluctuations in ROS, but ROS generation often exceeds the cell's antioxidant capacity, resulting in a condition termed oxidative stress. Host survival depends upon the ability of cells and tissues to adapt to or resist the stress, and repair or remove damaged molecules or cells. Numerous stress response mechanisms have evolved for these purposes, and they are rapidly activated in response to oxidative insults. Some of the pathways are preferentially linked to enhanced survival, while others are more frequently associated with cell death. Still others have been implicated in both extremes depending on the particular circumstances. In this review, we discuss the various signaling pathways known to be activated in response to oxidative stress in mammalian cells, the mechanisms leading to their activation, and their roles in influencing cell survival. These pathways constitute important avenues for therapeutic interventions aimed at limiting oxidative damage or attenuating its sequelae. Published 2002 Wiley‐Liss, Inc.

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NF-κB activation in response to toxical and therapeutical agents: role in inflammation and cancer treatment

Cited by 89 publications

References 69 publications

The inhibition of TNF-α-induced NF-κB activation by marine natural products

The inhibition of TNF-α-induced NF-κB activation by marine natural products

The Beneficial Effects of Morroniside on the Inflammatory Response and Lipid Metabolism in the Liver of <i>db</i>/<i>db</i> Mice

Cellular response to oxidative stress: Signaling for suicide and survival*

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