Effect of cis-resveratrol on genes involved in nuclear factor kappa B signaling

Leiro, J.; Arranz, Juan A.; Fraiz, Nuria; Sanmartín, M. L.; Quezada, Elías; Orallo, Francisco

doi:10.1016/j.intimp.2004.10.006

Cited by 86 publications

(49 citation statements)

References 57 publications

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“…RV was found to modulate the expression of genes associated with proinflammatory cytokines by up-regulating the nuclear factor of kappa light chain gene enhancer in IkappaBalpha and down-regulating NFkappaBL1. RV increased the pro-inflammatory cytokines interleukin-6 and TNF-alpha in sepsis (32). Consistent with these studies, we observed that RV treatment significantly increased GSH levels and decreased MDA levels in the liver and kidney of septic rats.…”

Section: Discussionsupporting

confidence: 90%

Resveratrol Protects Sepsis-Induced Oxidative DNA Damage in Liver and Kidney of Rats

Aydın¹,

Şahin²,

Bacanlı³

et al. 2016

Balkan Med J

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Background:The increases of free radicals have been proposed to be involved in the pathogenesis of sepsis, which leads to multiple-organ dysfunction syndromes. The uses of antioxidants as a complementary tool in the medical care of oxidative stress-related diseases have attracted attention of researchers. Resveratrol (RV) has suggested being antioxidant, anti-proliferative, and anti-inflammatory effects in various experimental models and clinical settings. Aims: This study was undertaken to evaluate the protective effects of RV on oxidative DNA damage induced by sepsis in the liver and kidney tissues of Wistar albino rats. Study Design: Animal experimentation. Methods: Four experimental groups consisting of eight animals for each was created using a total of thirty-two male Wistar albino rats. Sham group was given 0.5 mL of saline intra-peritoneal (ip) only following laparatomy. Sepsis group was given 0.5 mL saline ip only following the induction of sepsis. RV-treated group was given a dose of 100 mg/kg ip RV in 0.5 mL saline following laparatomy. RVtreated sepsis group was given 100 mg/kg ip RV in 0.5 mL saline following the induction of sepsis. A model of sepsis was created by cecal ligation and puncture technique. In the liver and kidney tissues, oxidative stress parameters (malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPX)) and a proinflammatory cytokine (tumor necrosis factor alpha (TNF-alpha)), were evaluated spectrophotometrically and DNA damage was determined by the alkaline single cell gel electrophoresis (comet assay) technique using formamidopyrimidine DNA glycosylase protein. Results:In the RV-treated sepsis group, the levels of MDA and TNF-alpha were lower and GSH levels, SOD and GPX activities were higher than in the septic rats (p<0.05). RV treatment significantly reduced the sepsis-induced oxidative DNA damage in the liver and kidney cells (p<0.05). Conclusion: It is suggested that RV treatment might reduce the sepsis-induced oxidative DNA damages in sepsis-related diseases; however, there is a need for more studies to clear up the protective mechanisms of RV against sepsis.

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Section: Discussionsupporting

confidence: 90%

Resveratrol Protects Sepsis-Induced Oxidative DNA Damage in Liver and Kidney of Rats

Aydın¹,

Şahin²,

Bacanlı³

et al. 2016

Balkan Med J

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“…Csiszar et al (2006) demonstraram em células endoteliais de artéria coronariana a inibição da expressão da IL-6, iNOS, ICAM-1, VCAM-1, bem como a menor ativação do NF-kB (mais de 50%) pelo resveratrol. Em macrófagos peritoniais estimulados com lipopolissacarídeo (LPS) e interferon-ã, o tratamento com cis-resveratrol bloqueou a expressão de genes relacionados à família Rel/NF-kB/IkB, às moléculas de adesão e a proteínas da fase aguda, bem como inibiu a expressão do receptor toll-like (TLR 3) e da MCP-1 (Leiro et al, 2005). Também se observa inibição da expressão do TNF-á pelo resveratrol (Bi et al, 2005).…”

Section: Mecanismos Moleculares De Ação De Polifenóis De Uvas E Vinhounclassified

Mecanismos moleculares de ação anti-inflamatória e antioxidante de polifenóis de uvas e vinho tinto na aterosclerose

Séfora-Sousa

Angelis-Pereira

2013

Rev. bras. plantas med.

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RESUMO:Este trabalho visa investigar os possíveis mecanismos moleculares de ação dos polifenóis de uvas e vinho tinto contra os processos oxidativos e inflamatórios envolvidos na aterosclerose. Trata-se de um estudo de revisão de literatura realizado por meio de buscas nas bases de dados PubMed e ScienceDirect utilizando os seguintes descritores: vinho tinto, uva, polifenóis, resveratrol, aterosclerose, LDL-oxidada, inflamação, estresse oxidativo, NF-kB, AP-1, Nrf2, SIRT-1, MicroRNA. Embora tais mecanismos ainda não estejam totalmente esclarecidos, os estudos indicam que compostos fenólicos presentes em uvas podem se complexar com metais (como ferro e cobre) que provocam peroxidação dos lipídios, aumentam a atividade antioxidante do plasma, associam-se com a LDL-c aumentando sua resistência à oxidação, preservam a atividade da enzima paraoxonase, neutralizam radicais livres, e ativam fatores de transcrição como o Nrf2, que aumenta a expressão de genes que codificam proteínas importantes na defesa antioxidante, como a superóxido dismutase e a glutationa peroxidase. Além disso, os polifenóis inibem a fosforilação de MAP quinases, inibindo assim os fatores de transcrição NF-kB e AP-1 e, consequentemente, reduzindo a síntese do TNF-á, interleucinas, moléculas de adesão e quimiocinas. Também inibem a atividade das enzimas cicloxigenase e lipoxigenase. Outro mecanismo proposto é a ação do resveratrol sobre a atividade de deacetilases de histonas, como a SITR-1. Estas ações em conjunto reduzem a oxidação da LDL-c e o processo inflamatório, atenuando o processo aterogênico. Palavras-chave:Resveratrol, LDL-c, Nrf2, NF-kB, AP-1, aterosclerose.ABSTRACT: Molecular mechanisms of action of grape and red wine polyphenols against oxidative and inflammatory processes in atherosclerosis. This study aimed to investigate the possible molecular mechanisms of action of grape and red wine polyphenols against oxidative and inflammatory processes in atherosclerosis. This is a literature review performed by searching in the PubMed and ScienceDirect databases using the following descriptors: red wine, grape, polyphenols, resveratrol, atherosclerosis, oxidized LDL, inflammation, oxidative stress, NF-kB, AP-1, Nrf2, SIRT-1, MicroRNA. Although the mechanisms are not fully understood, studies indicate that phenolic compounds possibly complex with metals (such as iron and copper), or else they increase the antioxidant activity of plasma and also preserve the activity of enzyme paraoxonase. Moreover, the polyphenols neutralize free radicals and activate transcription factors, for example Nrf2, which increases the expression of genes that encode important proteins in antioxidant defense (such as superoxide dismutase and glutathione peroxidase). Additionally, polyphenols inhibit the phosphorylation of MAP kinases, causing a blocking effect on the transcription factors NF-kB and AP-1 and, consequently, blocking the synthesis of TNF-α, interleukins, chemokines and molecules adhesion. Moreover, it can inhibit the activity of the cycloxygenase and li...

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“…83 A range of phytochemicals, including curcumin, epigallocatechin gallate (EGCG), resveratrol, guggulsterone, silibinin, zerumbone, indole-3-carbinol, and evodiamine, have been reported to inhibit activation of IκB kinase/NF-κB in cultured cells; the specific molecular targets of these agents, and the generality of their activity in this regard, remain unclear. 19,20,[104][105][106][107][108][109][110] Whether any of these compounds will achieve true clinical utility as NF-κB antagonists is somewhat doubtful, as it may not be feasible to achieve and maintain tissue concentrations comparable to those used in vitro; nonetheless, continuing research with these agents should be followed with interest. In particular, it is intriguing that orally administered silibinin can inhibit the growth of human prostate and lung cancers in nude mice; moreover, the sensitivity of the lung carcinoma to doxorubicin was amplified by silibinin.…”

Section: Complementary Strategies For Addressing Nf-kbmentioning

confidence: 99%

Preadministration of High-Dose Salicylates, Suppressors of NF-κB Activation, May Increase the Chemosensitivity of Many Cancers: An Example of Proapoptotic Signal Modulation Therapy

McCarty

Block

2006

Integr Cancer Ther

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NF-κB activity is elevated in a high proportion of cancers, particularly advanced cancers that have been treated previously. Cytotoxic treatment selects for such up-regulation inasmuch as NF-κB promotes transcription of a large number of proteins that inhibit both the intrinsic and extrinsic pathways of apoptosis; NF-κB also boosts expression of mdr1, which expels many drugs from cells. Indeed, high NF-κB activity appears to be largely responsible for the chemo-and radioresistance of many cancers. Thus, agents that suppress NF-κB activity should be useful as adjuvants to cytotoxic cancer therapy. Of the compounds that are known to be NF-κB antagonists, the most practical for current use may be the nonsteroidal anti-inflammatory drugs aspirin, salicylic acid, and sulindac, each of which binds to and inhibits IκB kinase-β, a central mediator of NF-κB activation; the low millimolar plasma concentrations of salicylate required for effective inhibition of this kinase in vivo can be achieved with highdose regimens traditionally used to manage rheumatic disorders. The gastrointestinal toxicity of such regimens could be minimized by using salsalate or enteric-coated sodium salicylate or by administering misoprostol in conjunction with aspirin therapy. Presumably, best results would be seen if these agents were administered for several days prior to a course of chemo-or radiotherapy, continuing throughout the course. This concept should first be tested in nude mice bearing xenografts of chemoresistant human tumors known to have elevated NF-κB activity. Ultimately, more complex adjuvant regimens can be envisioned in which salicylates are used in conjunction with other NF-κB antagonists and/or agents that target other mediators of down-regulated apoptosis in cancer, such as Stat3; coadministration of salicylate and organic selenium may have intriguing potential in this regard. These strategies may also have potential as adjuvants to metronomic chemotherapy, which seeks to suppress angiogenesis by targeting cycling endothelial cells in tumors.

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Effect of cis-resveratrol on genes involved in nuclear factor kappa B signaling

Cited by 86 publications

References 57 publications

Resveratrol Protects Sepsis-Induced Oxidative DNA Damage in Liver and Kidney of Rats

Resveratrol Protects Sepsis-Induced Oxidative DNA Damage in Liver and Kidney of Rats

Mecanismos moleculares de ação anti-inflamatória e antioxidante de polifenóis de uvas e vinho tinto na aterosclerose

Preadministration of High-Dose Salicylates, Suppressors of NF-κB Activation, May Increase the Chemosensitivity of Many Cancers: An Example of Proapoptotic Signal Modulation Therapy

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